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2 Acute inflammation Flashcards

1
Q

Definition of acute inflammation

A

protective rapid response of living tissue to injury

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2
Q

In the activation of the inflammatory process the tissue damage involves the detection of what ?

A

PAMPs/ DAMPS

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3
Q

In the activation of the inflammatory process with arachidonic acid mediators: activation of ..? formation of ..? a drug that inhibits the activation ?

A
  • activation of phospholipids (arachidonic acid released from cell membrane)
  • formation of inflammatory mediators (arachidonic acid mediators precursor of eicosanoid -> prostaglandins, thromboxanes, leukotrienes)
  • NSAIDs (ant-inflammatory effects, block conversion of arachidonic acid to prostaglandins and other eicosanoids )
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4
Q

6 examples of chemical mediators ?

A
  1. serotonin
  2. histamine
  3. complement
  4. bradykinin
  5. prostaglandin
  6. leukotrienes
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5
Q
  1. Endogenous chemical mediators are derived from where ?
  2. Example of exogenous chemical mediators
A
  1. plasma proteins, leucocytes and local tissues
  2. endotoxin from Gram negative bacteria
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6
Q

Key examples of increased vascular permeability chemical mediators ?

A
  • histamine
  • bradykinin
  • C5a + C5b
  • Nitric oxide
  • leukotrienes
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7
Q

Key examples of fever chemical mediators ?

A
  • IL-1
  • TNF
  • prostaglandins
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8
Q

List the 5 imaging investigations for acute inflammation

A
  • ECG
  • X-ray
  • CT (computed tomography)
  • MRI (magnetic resonance imaging)
  • U/S (ultrasound)
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9
Q

What is the most common occupational skin disease?

A

contact dermatitis

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10
Q

Among all the skin conditions related to work or occupational exposure, what is the most frequently encountered ?

A

contact dermatitis

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11
Q

what is inflammation of the skin known as ?

A

contact dermatitis

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12
Q

when does contact dermatitis occur ?

A

when skin comes into contact with irritants or allergens

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13
Q

In contact dermatitis how does the skin react ?

A

becomes:
* red
* itchy
* swollen
* blistered

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14
Q

Name an example of leukotriene antagonists (type of medication that blocks the effects of leukotrienes)

A

montelukast

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15
Q

What’s the disease with the complement deficiency in C1-inhibitor ?

A

hereditary angioedema

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15
Q

What 2 phases characterise acute inflammation ?

A

cellular and vascular phases

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16
Q

4 key features of acute inflammation & what is it initiated to limit [not the cardinal symptoms!]

A
  • immediate
  • short duration
  • innate (present from birth)
  • stereotyped (happens the same way no matter the cause of the inflammation )
  • initiated to limit tissue damage
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16
Q

5 clinical features of acute inflammation (cardinal symptoms)

A
  1. dolor - pain
  2. tumor - swelling
  3. rubor - redness
  4. calor - heat
  5. functio laesa - loss of function
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17
Q

In the activation of the inflammatory process with activation of kinin system , what gets formed ? what process ?

A
  • formation of bradykinin
  • vasodilation
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18
Q
  1. 2 examples of vasoactive amines ?
  2. example of vasoactive peptide ?
A
  1. histamine, serotonin
  2. bradykinin
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19
Q

What is the term inflammation not a synonym for ?

A

infection

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20
Q

what’s the suffix used to indicated inflammation of an organ or tissue ?

A

-itis

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21
Q

Give one example of an inflammation that doesn’t match the same suffix ending ?

A

pneumonia

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22
Q

List various factors that can cause or contribute to contact dermatitis + include examples

A

I F S I C

  • Irritants (such as soaps and detergents) - e.g. shampoos, bubble bath
  • food allergens - cows’ milk, egg, nuts
  • skin infections - staphylococcus aurues infectious is a common cause
  • inhalant allergens - dust mite
  • contact allergens - nickel, fagrances, propolis, poison ivy
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23
Q

Name an example of TNF alpha antagonists

A

Infliximab

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24
Q

What’s the disease with the complement deficiency in C3b-INA, C6, and C8 ?

A

severe neisseria infections

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25
Q
  1. What are endogenous chemical mediator groups derived from ?
  2. Example of exogenous chemical mediator group ?
A
  1. plasma-protein
  2. bacterial endotoxins
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26
Q

What 2 main types can inflammation be separated into ? Explain the differences between the 2 [CHANGE Q!!!]

A
  1. Acute -> develops quickly and lasts a few days
  2. Chronic -> can last for months or years, usually because of the persistence of the initiating factor
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27
Q

4 Infectious causes of inflammation

A
  • endotoxin from GN bacteria
  • PAMPs (all microorganisms)
  • enzymes
  • pathogens
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28
Q

7 non-infectious causes of inflammation

A

A F I T B I T

  • Allergens
  • Foreign bodies
  • Irritants e.g. nickel
  • Toxic compounds
  • Burns
  • Ionising radiation
  • Trauma and physical injury
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29
Q

key features of acute inflammation:
* …1… reactions
* controlled by ….2.. derived from …3..
* ..4.. but can lead to ..5.. and …6.. effects

A

1 = vascular + cellular
2 = a variety of chemical mediators derived
3 = plasma or cells
4 = protective
5 = local complications
6 = systemic effects

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30
Q

Give an example of the vascular and cellular reactions involved in acute inflammation

A

vasodilation + accumulation of fluid exudate and neutrophils in tissues

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31
Q

Give an overview of the events of acute inflammation

A
  1. tissue injury
  2. release of chemical mediators
  3. vasodilation
  4. exudate formation
  5. chemotaxis of neutrophils leukocytosis
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32
Q

examples of chemical mediators released after tissue injury in the event of acute inflammation

A
  • histamine
  • complement
  • kinin (blood pressure regulation)
  • prostaglandins
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33
Q

what process is exudate formation ?

A

process by which fluid, cells or other substances are released from blood vessels into nearby areas

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34
Q

what is chemotaxis of neutrophils leukocytosis ?

A

movement of cells in response to chemical signals

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35
Q

In the activation of the inflammatory process with complement activation what gets formed ?

A

MAC (membrane attack complex)

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36
Q

what do chemical mediators modulate ?

A

the inflammatory response

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37
Q

2 examples of chemokines (large family of chemotactic proteins) and cytokines (messengers) as chemical mediator groups

e.g. ..1… , …2..
made by ..3…
particularly made by ..4…

A
  1. IL-1
  2. TNF
  3. WBCs
  4. macrophages
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38
Q

Key examples of neutrophil chemotaxis, recruitment and activation chemical mediators ?

A
  • C5a
  • LTB4
  • bacterial peptides
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39
Q

Which stage of the infection cycle do symptoms first present, although vague ?

A

prodromal

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40
Q

List the 2 microbiological investigations for acute inflammation

  • if infectious susptected then…1….
  • ..2.. or other …3…..
A
  1. cultures
  2. PCR
  3. NAAT (polymerase chain reaction or other nucelic acid amplification tests)
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41
Q

List the 5 biochemical investigations for acute inflammation

A
  • renal profile
  • LFTs (liver function tests)
  • blood glucose
  • clotting tests
  • lactate
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42
Q
  1. Tonisilitis is usually caused by what pathogen ?
  2. Name 3 infectious that tonsilitis is most commonly caused by
A
  1. virus so it’s usually viral
  2. rhinovirus, coronavirus, adenovirus
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43
Q

Common bacterial pathogens related to tonsilitis include what ? what’s the most common ?

A

beta-haemolytic and other streptococci

most common = group A beta-haemolytic streptococci

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44
Q

Most cases of acute bronchitis are due to what ?

A

viral infections

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45
Q

What are the diseases to do with the complement deficiency of early C components C1, C4, C2 ?

A
  • systemic lupus erythematosus (SLE)
  • glomerulonephritis
  • polymyositis
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46
Q

5 steps of the activation of the inflammatory process ?

A
  1. tissue damage
  2. arachidonic acid (fatty acid that serves as a precursor for the synthesis of various bioactive lipid mediators) mediators
  3. activation of mast cells
  4. complement activation
  5. activation of kinin system
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47
Q

activation of the inflammatory process:

Tissue damage = detection of what ?

A

PAMPs/DAMPS

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48
Q

activation of the inflammatory process:

arachidonic acid mediators = activation of …1…, formation of…2…, drugs = …3…. ?

A
  1. phospholipids
  2. inflammatory mediators
  3. NSAIDs
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49
Q

activation of the inflammatory process:

activation of macrophages = degranulation and secretion of …1…, & ….2…..

A
  1. histamine
  2. vasodilation
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50
Q

activation of the inflammatory process:

complement activation = formation of …1…

A

MAC (membrane attack complex)

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51
Q

activation of the inflammatory process:

activation of kinin system = formation of …1… & …2…

A
  1. bradykinin
  2. vasodilation
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52
Q

What do chemical mediators modulate ?

A

inflammatory response

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53
Q

6 examples of chemical mediators

A
  • serotonin
  • histamine
  • complement
  • bradykinin
  • prostaglandin
  • leukotrienes
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54
Q

Chemical mediators can either be …. or …..

A

endogenous, exogenous

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55
Q

If chemical mediators are endogenous where are they derived from ?

A

plasma proteins, leukocytes, local tissues

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56
Q

where are chemical mediators that are exogenous from ?

A

endotoxin from gram negative bacteria

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57
Q

what is living duration of chemical mediators ?

A

short-lived

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58
Q

what does every chemical mediator have ?

A

an inhibitor

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59
Q

what are the 6 chemical mediator groups ?

A
  1. endogenous (cell-derived)
  2. vasoactive amines
  3. vasoactive peptides
  4. chemokines (large family of chemotactic proteins) and cytokines (messengers)
  5. arachidonic acid metabolites from plasma membrane phospholipids
  6. nitric oxide
60
Q

Arachidonic acid metabolites from plasma membrane phospholipids is one of the chemical mediator
groups give 3 examples of this

A
  • prostaglandins
  • leukotrienes e.g. LTB4
  • anti-inflammatory drugs (e.g. aspirin, NSAIDS, corticosteroids) working by inhibiting their synthesis
61
Q

Key examples of vasodilation chemical mediators ?

A
  • histamine
  • prostaglandins
  • bradykinin
  • Nitric oxide
62
Q

Key examples of phagocytosis chemical mediators ?

A

Fc (e.g. IgG antibody) & C3b = opsonins

63
Q

Key examples of itching + pain chemical mediators ?

A
  • bradykinin
  • serotonin
  • prostaglandins
64
Q

List 5 hematological investigations for acute inflammation

A
  • WBC count
  • FBC
  • CRP level (c-reactive protein level)
  • ESR (erythrocyte sedimentation rate)
65
Q

List the 2 specialised investigations for acute inflammation

A
  • CSF analysis e.g. meningitis
  • serology (lab medicine deals with detection of measurment of antibodies, antigens and other substances in the blood serum)
66
Q

List 5 disorders of acute inflammation

A
  • hereditary angio-oedema (swelling in deep layers of skin and other tissues)
  • alpha-1 antitrypsin deficiency
  • inherited complement deficiencies
  • defects in neutrophil function
  • defects in neutrophil numbers
67
Q
  1. Hereditary angioedema:
  2. how rare ?
  3. inheritance pattern ?
  4. deficiency of ? which is what ?
  5. types of oedema ?
  6. family history …?
A
  1. rare
  2. autosomal dominant
  3. C1 esterase inhibitor (a component of complement system)
  4. non-itchy cutaneous angio-oedema + laryngeal and/or intestinal oedema
  5. sudden death
68
Q

2 Types of oedema in hereditary angioedema

A

non-itchy cutaneous angio-oedema + laryngeal and/or intestinal oedema

69
Q

What’s the disease with the complement deficiency in C3 and factor B ?

A

severe bacterial infections

70
Q

Acute bronchitis can be …1…. despite most cases being due to viral infections give examples …2…

it is usually self-limiting

A
  1. non-infectious
  2. an inflammatory response to an irritant e.g. smoke, dust, fumes, pollutants
71
Q

What are the symptoms of acute bronchitis due to ?

A

acute inflammation of the bronchial wall causing increased mucus production together with production with oedema of the bronchus

72
Q

What are the 3 interrelated enzymatic cascade systems that produce inflammatory mediators in liver ?

A
  1. coagulation / fibrinolytic system: formation of thrombin + fibrin, activates 2 + 3
  2. kinin systems: produces bradykinin (vasoactive peptide) from plasma protein kininogens
  3. complement systems e.g. C5a, MAC, C3b
73
Q

The hallmark of a lower respiratory tract infection is the productive cough (sputum) what leads to this? [check and change?]

A

Acute inflammation of the bronchial wall, causes increased mucus production together with oedema of the bronchus

73
Q

List 5 examples of some anti-inflammatories

A
  • Aspirin / NSAIDs e.g. naproxen, ibuprofen
  • antihistamines
  • corticosteroids
  • leukotriene antagonists e.g. montelukast
  • TNF alpha antagonists e.g. infliximab
74
Q
  1. What condition is chronic granulomatous disease ?
  2. Neutrophils are unable to do what ?
  3. Chronic infections are present from when on ?
  4. numerous …. and abscesses
A
  1. genetic
  2. generate free radical superoxide so it can’t kill the bacteria by phagocytosis
  3. first year of life
  4. granulomas
75
Q

What is A1AT ?

A

a protease inhibitor which deactivates enzymes released from neutrophils during inflammation

76
Q

Alpha 1 antitrypsin deficiency:
1. inheritance pattern ?
2. low levels of ..?
3. A1AT = is what ?
4. what goes unchecked ?
5. as well as cirrhosis what else ?

A
  1. autosomal recessive
  2. low levels
  3. protease inhibitor which deactivates enzyme released from neutrophils during inflammation
  4. inflammation and enzymatic destruction of tissues
  5. emphysema
77
Q

After tissue injury, next is release of chemical mediators list 4 of the chemical mediators released

A
  1. histamine
  2. complement
  3. kinin (blood pressure regulation)
  4. prostaglandins
78
Q

4 sequelae of acute inflammation ?

A
  • resolution
  • suppuration (excess exudate)
  • chronic inflammation (persistent causal agent)
  • death
79
Q

Resolution as sequelae of acute inflammation:

Mediators have …1… half lives, degraded quickly after release, damaged cells ..2… if tissue damage …3…..

Neutrophils have a …4… half life.

…5… removal of stimulus, …6….. which drains to lymphatics and debris.

…7…. broken down by ….8….. process (plasmin and other proteases)

A
  1. short
  2. regenerate
  3. minimal
  4. short
  5. rapid
  6. exudate
  7. fibrin
  8. thromolytic
80
Q

suppuration (excess exudate) as sequelae of acute inflammation:

Formation of ..1…., a mixture of dying neutrophils, bacteria and cellular debris.

Usually …2…. / persistent bacterial infection.

Can become walled off by a ‘….3…. membrane’, …4….. formation.

Inaccessible to ….5…. + …6…. system.

A
  1. pus
  2. infective
  3. pyogenic
  4. abscess
  5. antibiotics
  6. immune
81
Q

chronic inflammation (persistent causal agent) as sequelae of acute inflammation:
* ….1….repair
* …..2…. and tissue organisation
* …..3…..tissue formation

A
  1. fibrous
  2. scarring
  3. granulation
82
Q
  1. where is hypovolaemic shock often seen in ?
  2. seen due to what ?
A
  1. burns
  2. insufficient blood flow or excessive injury
83
Q

what can septic shock occur due to ?

A

overwhelming systemic infection resulting in vasodilation leading to hypotension

84
Q

Obstructive shock seen in cardiac tamponade , what does the fluid do ?

A

fluid in the pericardium prevents venous return

85
Q

type IV hypersensitivty reactions …
1. mediated by ?
2. time frame ?

A
  1. T cells
  2. delayed (24 to 72 hours)
86
Q

Type III hypersensitivity is..
1. mediated by ?
2. time frame ?

A
  1. antigen-antibody imune complexes
  2. hours to days/weeks
87
Q

examples of type IV hypersensitivity reactions?

A
  1. contact dermatitis
  2. tuberculin skin test
88
Q

examples of type III hypersensitivity reactions

A
  • serum sickness
  • RA
  • SLE
  • post-streptococcal glomerulonephritis
89
Q

examples of Type II hypersensitivity reactions

A
  • haemolytic disease of the newborn
  • autoimmune haemolytic anaemia
  • goodpasture’s syndrome
90
Q

Type II hypersensitivity :
1. mediated by ?
2. time frame ?

A
  1. IgG or IgM antibody (cytotoxic)
  2. hours to days
91
Q

Type I hypersensitivity is :
1. mediated by ?
2. timeframe ?

A
  1. IgE antibody
  2. immediate (minutes)
92
Q

3 examples of type I hypersensitivity reactions

A
  • allergy
  • anaphylaxis
  • atopy
93
Q

sensitisation to an allergen on re-exposure can develop ….1…. reaction

….2…. infection or long term exposure can lead to …3…. complexes

A
  1. hypersensitivity
  2. persistent
  3. antigen-antibody
94
Q

Airway swelling in acute epiglottis results in raised ..1.., ..2… herniation / coning in acute bacterial …3… due to obstruction of CSF channels

A
  1. ICP
  2. tonsillar
  3. meningitis
95
Q

List 6 examples of local complications

A
  • Swelling
  • Inappropriate inflammation
  • Exudation of fluid e.g. pericardial space following MI -> tamponade (prevents pumping of heart)
  • Loss of fluid, shock e.g. burns
  • Prolonged pain and loss of function
  • Digestion of host tissues by harmful enzymes released by neutrophils e.g. vascular damage in glomerulonephritis.
96
Q

Systemic effect of shock = circulatory failure (clinical syndrome) ,
1. what is it due to ?
2. often …. ?

A
  1. spread of microorganisms and toxins (septic shock)
  2. fatal
97
Q

List 5 acute phase proteins released from the liver

A
  • fibrinogen
  • CRP (C-reactive protein)
  • alpha1 antitrypsin
  • Haptoglobin
  • Serum amyloid A protein
98
Q

how does pain and loss of function combat injury ?

A

enforces rest, reduces chance of further traumatic damage

99
Q

How does infiltration of inflammatory cells combat injury ?

A

removes pathogenic organisms, necrotic debris

100
Q

How does vasodialtion combat injury ?

A

increases delivery, increases temperature

100
Q

How does the exudation of fluid combat injury ?

A
  1. delivers plasma proteins, immunoglobulins and inflammatory mediators e.g. fibrinogen to area of injury
  2. oedema elicits increased lymphatic drainage ; delivers antigens to immune system (lymph nodes) as well as microorganisms to phagocytes
  3. serves to dilute toxins reducing impact
101
Q

Hallmark of acute inflammation loss of function results from what ?

A

loss of mobility due to oedema, pain or replacement of cells

102
Q

Hallmark of acute inflammation heat results from what ?

A

vasodilation

103
Q

Hallmark of acute inflammation swelling results from what ?

A

oedema, exudate due to vasodilation and increased permeability of blood vessels

104
Q

Hallmark of acute inflammation pain results from what ?

A

bradykinin, prostaglandins released

105
Q

Hallmark of acute inflammation redness ‘rubor’ results from what ?

A

vasodilation in vascular phase (more blood flow)

106
Q

Summarise the role of neutrophils in acute inflammation

A
  1. neutrophils migrate to site of injury by chemotaxis
  2. phagocytose and kill microorganisms
  3. eliminate foreign material and necrotic tissue
  4. produce growth factors for repair
  5. degranulation
  6. release of pro-inflammatory cytokines
106
Q

Toxic oxygen species is converted to hydrogen peroxide by …1…. from neutrophil granules

…2…. - halide system -> hypochlorite

A
  1. myeloperoxidase
  2. H2O2-myeloperoxidase
107
Q

The debris from a phagocyte are released by exocytosis, engulfed cells can be killed in one of 2 ways what are these 2 ways ?

A
  • oxygen dependent mechanisms
  • oxygen independent mechanisms
108
Q

Oxygen dependent mechanism:
1. what’s released into the phagosome ?
2. mechanism of killing known as ?

A
  1. oxygen derived free radicals
  2. oxidative burst
109
Q

oxygen independent mechanisms :
1. what is used to kill bacteria inside the phagolysosome ?
2. examples of this ‘what’
3. what can form holes in microbial membranes ?

A
  1. enzymes
  2. proteases, lipases, nucleases
  3. nucleases from neutrophil granules
110
Q

what are the 4 steps of phagocytosis ? use bacterium as an example

A
  1. neutrophil ingests the bacterium
  2. bacterium lies within a phagosome
  3. lysosomes fuse with phagosome and enzymes digest the bacterium (phagolysosome)
  4. bacterial debris released from neutrophil and lysosomes replenished
111
Q

what is margination ?

A

neutrophils move towards the endothelial wall where they then roll along it until they become trapped, when they become trapped, they then crawl out of the vessel

112
Q

What are the 6 steps that neutrophils infiltrate the tissue and attach to bacteria ?

A
  1. chemotaxis
  2. activation
  3. margination
  4. diapedesis
  5. recognition attachment
  6. phagocytosis
113
Q

Chemotaxis = 1st step that neutrophils infiltrate the tissue and attach to bacteria

explain what it is ?

A

neutrophils attracted towards the site of injury by chemical attractants

114
Q

activaiton = 2nd step that neutrophils infiltrate the tissue and attach to bacteria

explain what it is ?

A

neutrophils switch to a higher metabolic level and change shape to help them move towards the chemical attractant

115
Q

margination = 3rd step that neutrophils infiltrate the tissue and attach to bacteria

explain what it is ?

A

neutrophils move towards the endothelial wall where they then roll along it until they become trapped, when they become trapped, they then crawl out of the vessel

116
Q

diapedesis = 4th step that neutrophils infiltrate the tissue and attach to bacteria

explain what it is ?

A

neutrophils relax the junctions between the endothelial cells so they can move across the endothelium

they also use collagenase to break down the basement membrane

117
Q

recognition attachment = 5th step that neutrophils infiltrate the tissue and attach to bacteria

explain what it is ?

A

neutrophils recognise the bacterium via the opsonins which attract to the bacterium

neutrophils then move towards and attach to the bacterium

118
Q

phagocytosis = 6th step that neutrophils infiltrate the tissue and attach to bacteria

explain what it is ?

A

process by which neutrophils engulf and destroy the bacteria

119
Q

Inflammation is the …1…of any …2….tissue in order to deliver various …3… materials such as white blood cells and proteins to the site of injury. The purpose of inflammation is to defend against ….4…..and to clear …5…..

A
  1. rapid response to injury
  2. vascularised living
  3. defensive
  4. infection
  5. damaged tissue
120
Q

What are the 4 stages that acute inflammation can be broken down into ?

A
  • Stimulus e.g. infection, truama or chemical agents.
  • Vascular stage - slowing the local circulation and forming exudate at the site of inflammation.
  • Cellular stage - the migration of neutrophils to the site.
  • Either resolution where the tissue returns to normal, or persistence which can lead to chronic inflammation.
121
Q

How do neutrophils escape from vessels ?

A
  • relaxation of inter-endothelial cell junctions
  • digestion of vascular basement membrane
  • movement
121
Q

List examples of chemotaxins in the stage of diapedesis

A
  • C5a
  • LTB4
  • cytokines (endogenous)
  • bacterial products (exogenous)
  • clotted blood
122
Q

What are the receptors/ chemical mediators at the diapedesis stage of neutrophil extravasation ?

A
  • chemotaxins
  • e.g. C5a, leuktriene B4, bacterial peptides
  • stimulate neutrophils to migrate through the inter-endothelial cell junctions
123
Q

What are the receptors/ chemical mediators at the adhesion stage of neutrophil extravasation ?

  1. Integrins expressed by neutrophils bind to …. on the endothelium
  2. ….., leukotriene B4, …. and …. increase expression
A
  1. integrin ligands
  2. C5a, IL-1, TNF
124
Q

What are the receptors/ chemical mediators at the rolling stage of neutrophil extravasation ?

  1. selectins expressed by endothelial cells bind to …. on neutrophils
  2. increased by …. secreated by …. e.g.
A
  1. selectins expressed by endothelial cells bind to carbohydrate ligands (sLex) on neutrophils
  2. increased by several cytokines secreted by macrophages, mast cells and endothelial cells e.g. IL-1 and TNF
125
Q

What are the 4 steps of neutrophil extravasation ?

A
  1. vascular stasis causes neutrophils to line up along endothelium = margination
  2. roll along endothelium = rolling
  3. stick avidly to endothelium = adhesion
  4. emigrate through the endothelium = migration / diapedesis
126
Q

what are neutrophils also known as ?

A

primary leukocyte = neutrophil (also known as neutrophil leukocyte, neutrophil polymorph, PMN, polymorph)

127
Q

neutrophils are ….1… cells involved in …2…inflammation , they are type of ….3…, first …..4…. hrs, …5…-lived

A
  1. wbc
  2. acute
  3. granulocyte
  4. 6-24
  5. short
128
Q

List 4 types of exudate (fluid with high protein content e.g. acute inflammation) and an example where found ?

A
  1. purulent e.g. meningitis
  2. haemorrhagic/serosanguinous e.g. malignancies or trauma
  3. serous, clear (maybe transudate or exudate) e.g. blister
  4. fibrinous e.g. fibrinous pericarditis
129
Q

In heart failure although increased …1… pressure the vessel is …2… and don’t leak …3… proteins so ..4… osmotic pressure is static

A
  1. hydrostatic
  2. intact
  3. plasma
  4. colloid
130
Q

What are the 2 main types of fluids that can accumulate in body cavities or tissues due to various pathological processes ? what’s the difference between the 2 fluid types ?

A
  1. transudate = fluid with low protein content
  2. exudate = fluid with high protein content e.g. acute inflammation
131
Q

What are the 3 main components of inflammation ?

A
  1. an increase in the blood supply to the affected area, caused by dilation of arterioles supplying the area
  2. an increase in the permeability of capillaries, allows larger serum molecules e.g. antibodies to enter the tissue
  3. migration of leukocytes from blood into the tissues - leukocytes cross the endothelial cells, which line the venules and then move out into the tissue
132
Q

what are the 2 phases of acute inflammation ?

A

vascular & cellular

133
Q

what are the changes in tissue that happen in the vascular & cellular phases of acute inflammation ?

A

vascular: changes in blood blow (INC blood flow) , exudation of fluid into tissues

cellular: infiltration of inflammatory cells

134
Q

What modulates the changes in tissue of vascular & cellular phases of acute inflammation

A

different inflammatory mediators modulate these steps

135
Q

Vascular phase: mechanisms of vascular leakage exudation occurs as a result of several mechanisms:

A
  1. endothelial contraction
  2. cytoskeletal reorganisation
  3. direct injury
  4. leukocyte-dependent injury
  5. increased transcytosis
136
Q

Exudate fluid allows what like firbin to happen ?

A

plasma proteins to be delivered directly to the injury site

137
Q

What is endothelial contraction mediated by ?

A

histamine and leukotrienes

138
Q

what is cytoskeletal reorganisation mediated by ?

A
  • cytokines
  • IL-1
  • TNF-alpha
139
Q

Direct injury from …1…. or …2…. is one mechanism of vascular leakage exudation

A

toxic burns , chemicals

140
Q

leukocyte-dependent injury may happen due to what ?

A

toxic oxygen species or enzymes from leukocytes

141
Q
  1. what is transcytosis ?
  2. mediated by what ?
A
  1. channels across endothelial cytoplasm
  2. VEGF
142
Q

In the vascular phase of acute inflammation - changes in blood flow what happens ?

A)….1….. vasoconstriction of arterioles (very …..2…..)

B) Followed by …..3….. of arterioles and then …4…. -> ….5…… blood flow

C) .↑vascularpermeability ->…6…. of protein- rich fluid into tissues and …7…. of circulation

D) Vascular …8…. (because blood more viscous due to increased ….9…. of red cells in vessels from leaked fluid)

A
  1. transient
  2. short
  3. vasodilation
  4. capillaries
  5. INC
  6. exudation
  7. slowing
  8. stasis
  9. concentration
143
Q

Systemic effects of acute response in liver :

Constitutional symptoms (symptoms that affect entire body rather than specific organ ) (…1….)

–…2…. phase proteins: fibrinogen, CRP (C-reactive protein), alpha1 antitrypsin, Haptoglobin, Serum amyloid A protein

– reduced …3….synthesis

A
  1. malaise, anorexia, nausea
  2. acute
  3. protein
144
Q

Systemic effects leukocytosis (INC WCC):

…1… cells release …2…-stimulating factors
so bone marrow produces more …3….

– IL-1 and …4…. accelerate release from Bone Marrow
– Bacterial infections = ↑…5….
– viral = ↑…6….

A
  1. macrophages + endothelial
  2. colony
  3. leukocytes
  4. TNF alpha
  5. neutrophils
  6. lymphocytes
145
Q

Systemic effects pyrexia involves:

A) ..1…. endotoxins

B) …2….cytokines e.g. TNF-alpha, IL-2, from macrophages and neutrophils act on …3…. hypothalamus, INC synthesis of ….4…. (reason why aspirin reduces fever)

A
  1. bacterial
  2. pyrogenic
  3. anterior
  4. prostaglandins E2

MOD (22 decks)

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