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Pathological Processes > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Define inflammation

A

The response of living tissue to injury

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2
Q

What are features of acute inflammation?

A
  • immediate response
  • short duration ( minutes to hours )
  • innate ( an inbuilt mechanism that is always the same)
  • limits damage
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3
Q

What causes inflammation ?

A

1) trauma / foreign body

2 ) microorganisms

3) hypersensitivity ( eg pollen , gluten )
4) other illnesses eg necrosis

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4
Q

What are the clinical signs of acute inflammation ?

A

1) RUBOR - redness
2) CALOR : heat
3) TUMOR : Swelling
4) DOLOR : pain
5) Loss of function

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5
Q

What are the 4 phases of acute inflammation ?

A

1) vascular phase
2) cellular phase
3) controlled
4) protective phase

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6
Q

Outline the vascular phase of acute inflammation?

A

1) firstly , vasoconstriction occurs. This lasts for seconds.
2) secondly , vasodilation occurs. This lasts for minutes. This allows more blood to flow through the vessel. This accounts for the redness ( rubor) and heat ( calor).
3) thirdly , there is an increased permeability in the vessels which allows fluid and cells to escape.

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7
Q

What does starlings law state ?

A

Movement of fluid is controlled by the balance of hydrostatic pressure and oncotic pressure

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8
Q

What does hydrostatic pressure term to

A

The pressure exerted on a vessel wall by fluid

  • this pushes fluid AWAY
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9
Q

What does oncotic pressure term to

A

The pressure exerted by proteins. This draws fluid towards a vessel.

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10
Q

Where does hydrostatic pressure and oncotic pressure exist ?

A

In the vessels and the interstitium

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11
Q

During vasodilation , what occurs to the hydrostatic pressure ?

A

The hydrostatic pressure increases in a capillary blood vessel this is because there is more blood flowing through the vessel.

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12
Q

During the acute inflammation stage , where there is an increased vessel permeability what occurs to the oncotic pressure ?

A

Interstitium oncotic pressure increases as more plasma proteins such as albumin move into the interstitum

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13
Q

As a result of vessel permeability increasing and vasodilation occurring , what is the overall effect of the movement of fluid ?

A

There will be an increased amount of fluid movement of a vessel into the interstitium. This results in OEDEMA. ( swelling /tumor)

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14
Q

As there is an increased movement of fluid out of. A vessel , what occurs to the blood ?

A

This increases viscosity of blood

Which reduces flow through vessel ( STASIS)

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15
Q

Define stasis

A

Reduced flow through vessel

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16
Q

What are the two types of interstitial fluid ?

A

1) exudate

2) transudate

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17
Q

What is exudate interstitial fluid ?

A
  • there is an increased vascular permeability
    2) protein rich fluid.
    3) occurs during inflammation
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18
Q

What is transudate interstitial fluid ?

A

1) vascular permeability unchanged
2) not related to inflammation
3) fluid movement due to increased capillary hydrostatic pressure and reduced capillary oncotic pressure.
4) this is often related to heart failure( this increases hydrostatic pressure). Hepatic failure ( this causes a decrease is plasma proteins which is accountable for the reduction in oncotic pressure). And renal failure.

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19
Q

In an exudate interstitial fluid , would you find red and white cells ?

A

You will find VERY FEW white and red cells

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20
Q

What are the three ways a vessel wall may become permeable ?

A

1) retraction of endothelialncells ( caused by histamine , leukotrienes, nitric oxide) the cells separate which allows a gap between the endothelial cells to form.
2) DIRECT INJURY : by burns , toxins or direct trauma which damages the vessels
3) leucocyte dependant injury : these leucocytes release toxic oxygen species such as free radicals or even enzymes that damage the endothelial wall.

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21
Q

Why is the vascular phase effective ?

A

1) the interstitial fluid diluted toxins
2) the exudate delivers proteins for example FIBRIN which produces mesh that limits spread of toxins. Also immunoglobins are released by lymphocytes

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22
Q

How is the fluid removed ?

A

By lymph nodes - these lymph nodes contain lymphocytes which proliferate to try and fight injections too. This is why lymph nodes may swell and appear in certain areas of our body ( cervical , axillae )

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23
Q

What is the primary white blood cell involved in acute inflammation ?

A

Neutrophils

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24
Q

Describe the appearance of white blood cells eg neutrophils

A

They are TRILOB- lots of dotted cytoplasm

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25
Q

Outline the process of the cellular phase

A

1) the neutrophils escape the vessels with the aid of adhesion molecules
2) neutrophils move through the interstitium via the process of chemotaxis
3) neutrophils phagocytose pathogens through a specific recognition process and two killing mechanisms

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26
Q

How do neutrophils escape vessels ?

A

Step 1 : MARGINATION - the neutrophils move to ends of the blood vessels because of the increase In viscosity.

  1. They begin to role along the endothelial cells with the help of ‘ SELECTINS’ which are cells expressed in activated endothelial cells. SELECTINS are adhesion molecules.
    3) Integrins which are found on the neutrophil surface change from low affinity to high affinity state once bound to endothelial cell . This allows tight binding. This is responsible for adhesion.
    4) neutrophils them emigrate out of vessel. ( diapedesis). They don’t use the endothelial gaps through which the exudate escapes. Instead they produce collagenase which digests the basement membrane .
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27
Q

How do neutrophils move through the interstitium?

A

Through a process called chemotaxis

  • this is the directional movement of a neutrophil towards a chemical attractant ( chemotaxin)
  • neutrophils move UP a chemotactic gradient.
  • chemotaxins involve bacterial products , spilled blood , injured tissues. For example an endotoxin, this is a lipopolysaccharide from the outer membrane of a gram negative bacteria.
  • activation of the complement system releases fragments of C3, C4 and C5 etc etc which are all chemotactic
28
Q

Once neutrophils have entered the interstitium, what do they do to the pathogens ?

A

PHAGOCYTOSIS

29
Q

Outline the process of phagocytosis

A

1) phagocytes engulf pathogen
2) this forms a phagosome
3) lysosomes fuse with the phagosome to form a secondary phagolysosomes
4) pathogen broken down into soluble debris which is this exocytosed.

30
Q

How do neutrophils know what to phagocyttose ?

A

Through a process called opsonisation

  • pathogen gets covered in opsonins- which are plasma proteins ( eg C3B of Fc). These neutrophils have corresponding receptors to these opsonins.
  • these opsonins ( C3B or Fc) are released from the complement system.
  • another important opsonin is IgG antibody but it will not be present when a bacterium is encountered for the first time.
31
Q

What are the two mechanisms for neutrophils to destroy pathogens ?

A

1) OXYGEN DEPENDANT

2) OXYGEN INDEPENDANT

32
Q

What is the oxygen dependant mechanism for killing pathogens ?

A
  • it involves the rapid release of reactive oxygen intermediates such as superoxide ( O2-) , OH, h202. And reactive nitrogen intermediates such as NO and NO2. These are involved in the process of respiratory burst.
33
Q

What is the oxygen independant mechanism for killing pathogens ?

A
  • the process of killing pathogens through lysosomes , hydrolytic enzymes , and defensins
34
Q

Why is the cellular phase effective ?

A

1) REMOVES PATHOGENS AND NECROTIC CELLS

2) RELEASES INFLAMMATORY MEDIATORS ( this can happen through phagocytosis )

35
Q

Define inflammatory mediators

A

They are chemical messengers which control and co-ordinate the inflammatory response.

  • they originate from activates inflammatory cells , platelets , endothelial cells and toxins.
36
Q

Give examples of inflammatory mediators that is released to bring about vasodilation

A
  • histamine
  • serotonin
  • prostaglandins
  • nitric oxide
37
Q

Give examples of inflammatory mediators that are released to induce an increase in permeability in blood vessels

A
  • histamine
  • C3a and C5a
  • bradykinin
  • leukotrienes
38
Q

Give examples of inflammatory mediators that induce chemotaxis of neutrophils

A
  • IL-1
  • TNF-a
  • C5a
  • bacterial peptide
39
Q

Give examples of inflammatory mediators that induce fever

A

PYROGENS : for example prostaglandins, IL-1, IL-6 , TNF-a

40
Q

What are examples of inflammatory editors that induce pain ?

A
  • prostaglandins
  • bradykinin
  • substance p
41
Q

What are the disadvantages of acute inflammation ?

A

Could lead to local or systemiccomplications

42
Q

What are examples of local complications due to acute inflammation ?

A

1) SWELLING: which results in compression of tubes for example , the airways m bile duct , intestine
2) A build of exudate in in the pericardial sac could compress the heart. This results in cardiac tamponade. This reduces ventricular filling.
3) LOSS of fluid: for example in burns there could be a loss of fluid. A lot of times , people with burns die of dehydration.
4) PAIN: muscular atrophy , physco -social consequences

43
Q

What are examples of systemic complications ?

A

1) FEVER : inflammatory mediators such a spyrogen are released. These act on the hypothalamus which work to alter temperature.
2) LEUCYTOSIS : increased production of white cells.
3) Reduced appetite , tachycardia , altered sleep. This all induces rest.
4) SEPTIC SHOCK : huge release of chemical mediators which causes widespread vasolidilation. This causes hypotension , tachycardia. Multi organ failure .

44
Q

If there are more neutrophils than lymphocytes what does this indicate ?

A

Bacterial infection

45
Q

If there are more lymphocytes than neutrophils , what does this indicate ?

A

Viral infection

46
Q

What are the three things that can occur after acute inflammation ?

A

1) complete resolution
2) repair with connective tissue
3) progression to chronic inflammation

47
Q

After acute Inflammation , how does the body restore itself ?

A

1) mediators have short half lives this causes get diluted or inactivated.
2) vessel Calibre and permeability returns to normal
3) neutrophils undergo apoptosis and get phagocytosed
4) exudate drained via the lymphatic system

5)

48
Q

How does the body get repaired with connective tissue after acute inflammation?

A

Fibrosis occurs which is the excess production of fibrous connective tissue in an organ or tissue in reparative process. This occurs when there has been substantial tissue destruction.

49
Q

When does progression to chronic inflammation occur !

A
  • when acute inflammation was not an adequa response to the stimuli which results in progression to chronic,
50
Q

What is the suffix for inflammation ?

A

ITIS

51
Q

What causes inflammation of the appendix ? ( appendicitis)

A
  • blockage of the lumen of appendix. By ‘ faecolith’. Blockage by a faeces rock.
  • this results in commensals proliferating + exudate levels increasing, this causes an increased in pressure.
52
Q

What causes penuemonia?

A

Main causative organisms : streptococcus pneumoniae

  • haemophilus infleunzae
  • this results in a build up of exudate between the layers of the pleura.
53
Q

What is pneumonia?

A

Lower respiratory tract infection

54
Q

What are the signs and symptoms of pneumonia?

A

Shortness of breath

Cough

Sputum

Fever

55
Q

What are the risk factors for pneumonia?

A

Smoking

Pre existing lung condition such as asthma , COPD, malignancy

56
Q

What is bacterial meningitis ?

A

Inflammation of the meninges ( membranous covering of the brain and spinal cord )

57
Q

What causes bacterial meningitis ?

A

Neisseria meningitdes

E. coli

Group H streptococcus

58
Q

What are signs of symptoms of bacterial meningitis?

A

Headache

Neck stiffness

Photophobia

Altered mental state

59
Q

What are the three examples of inflammation of the serous cavities ? ( exudate pours into the serous cavities)

A

1) exudate pours into the pleural space : pleural effusion? A common sign of pneumonia
2) Exudate pours into the peritoneal space = ASCITIES. This is a common symptom of the alcoholic liver disease,
3) Exudae pours into the pericardial space = PERICARDIAL EFFUSION.

60
Q

What are three disorders of acute inflammation ?

A

1) hereditary Anglo-oedema
2) alpha - 1- antitrypsin deficiency
3) chronic glanilpmatous disease

61
Q

What are the four pathological stages of pneumonia

A

1) congestion
2) Red hepatization
3) Grey hepatization
4) resolution

62
Q

What occurs during the congestion stage of pneumonia?

A
  • this occurs within the first 24 hours
  • this is where there is vascular dilation ,so there is a lot of exudate in the alveolar space which mainly contains bacteria.
  • the lobe looks red , heavy and boggy
63
Q

What occurs during red hepatization?

A
  • this occurs during the 2-3 rd day.
  • the lobe appears red , airless
  • the alveolar exude contains neutrophils , erythrocytes , fibrin.
64
Q

What occurs during gray hepatization?

A
  • this occurs 4-6th day.
  • the lobe appears grey - brown
  • this occurs when the RBC are fragmented / begin to lyse
  • the alveolar exudate contains neutrophils , fibrin
65
Q

What occurs during the resolution stage of pneumonia?

A
  • this occurs after 6 days
  • the normal architecture of the lungs are restored
  • enzymatic digestion of the exudate occurs.

Pathological Processes (13 decks)

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