2 Acute inflammation Flashcards
(151 cards)
1
Q
Definition of acute inflammation
A
protective rapid response of living tissue to injury
2
Q
In the activation of the inflammatory process the tissue damage involves the detection of what ?
A
PAMPs/ DAMPS
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 )
4
Q
6 examples of chemical mediators ?
A
- serotonin
- histamine
- complement
- bradykinin
- prostaglandin
- leukotrienes
5
Q
- Endogenous chemical mediators are derived from where ?
- Example of exogenous chemical mediators
A
- plasma proteins, leucocytes and local tissues
- endotoxin from Gram negative bacteria
6
Q
Key examples of increased vascular permeability chemical mediators ?
A
- histamine
- bradykinin
- C5a + C5b
- Nitric oxide
- leukotrienes
7
Q
Key examples of fever chemical mediators ?
A
- IL-1
- TNF
- prostaglandins
8
Q
List the 5 imaging investigations for acute inflammation
A
- ECG
- X-ray
- CT (computed tomography)
- MRI (magnetic resonance imaging)
- U/S (ultrasound)
9
Q
What is the most common occupational skin disease?
A
contact dermatitis
10
Q
Among all the skin conditions related to work or occupational exposure, what is the most frequently encountered ?
A
contact dermatitis
11
Q
what is inflammation of the skin known as ?
A
contact dermatitis
12
Q
when does contact dermatitis occur ?
A
when skin comes into contact with irritants or allergens
13
Q
In contact dermatitis how does the skin react ?
A
becomes:
* red
* itchy
* swollen
* blistered
14
Q
Name an example of leukotriene antagonists (type of medication that blocks the effects of leukotrienes)
A
montelukast
15
Q
What’s the disease with the complement deficiency in C1-inhibitor ?
A
hereditary angioedema
15
Q
What 2 phases characterise acute inflammation ?
A
cellular and vascular phases
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
16
Q
5 clinical features of acute inflammation (cardinal symptoms)
A
- dolor - pain
- tumor - swelling
- rubor - redness
- calor - heat
- functio laesa - loss of function
17
Q
In the activation of the inflammatory process with activation of kinin system , what gets formed ? what process ?
A
- formation of bradykinin
- vasodilation
18
Q
- 2 examples of vasoactive amines ?
- example of vasoactive peptide ?
A
- histamine, serotonin
- bradykinin
19
Q
What is the term inflammation not a synonym for ?
A
infection
20
Q
what’s the suffix used to indicated inflammation of an organ or tissue ?
A
-itis
21
Q
Give one example of an inflammation that doesn’t match the same suffix ending ?
A
pneumonia
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
23
Name an example of TNF alpha antagonists
Infliximab
24
What's the disease with the complement deficiency in C3b-INA, C6, and C8 ?
severe neisseria infections
25
1. What are endogenous chemical mediator groups derived from ?
2. Example of exogenous chemical mediator group ?
1. plasma-protein
2. bacterial endotoxins
26
What 2 main types can inflammation be separated into ? Explain the differences between the 2 [CHANGE Q!!!]
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
27
4 Infectious causes of inflammation
* endotoxin from GN bacteria
* PAMPs (all microorganisms)
* enzymes
* pathogens
28
7 non-infectious causes of inflammation
A F I T B I T
* Allergens
* Foreign bodies
* Irritants e.g. nickel
* Toxic compounds
* Burns
* Ionising radiation
* Trauma and physical injury
29
key features of acute inflammation:
* ...1... reactions
* controlled by ....2.. derived from ...3..
* ..4.. but can lead to ..5.. and ...6.. effects
1 = vascular + cellular
2 = a variety of chemical mediators derived
3 = plasma or cells
4 = protective
5 = local complications
6 = systemic effects
30
Give an example of the vascular and cellular reactions involved in acute inflammation
vasodilation + accumulation of fluid exudate and neutrophils in tissues
31
Give an overview of the events of acute inflammation
1. tissue injury
2. release of chemical mediators
3. vasodilation
4. exudate formation
5. chemotaxis of neutrophils leukocytosis
32
examples of chemical mediators released after tissue injury in the event of acute inflammation
* histamine
* complement
* kinin (blood pressure regulation)
* prostaglandins
33
what process is exudate formation ?
process by which fluid, cells or other substances are released from blood vessels into nearby areas
34
what is chemotaxis of neutrophils leukocytosis ?
movement of cells in response to chemical signals
35
In the activation of the inflammatory process with complement activation what gets formed ?
MAC (membrane attack complex)
36
what do chemical mediators modulate ?
the inflammatory response
37
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...
1. IL-1
2. TNF
3. WBCs
4. macrophages
38
Key examples of neutrophil chemotaxis, recruitment and activation chemical mediators ?
* C5a
* LTB4
* bacterial peptides
39
Which stage of the infection cycle do symptoms first present, although vague ?
prodromal
40
List the 2 microbiological investigations for acute inflammation
* if infectious susptected then...1....
* ..2.. or other ...3.....
1. cultures
2. PCR
3. NAAT (polymerase chain reaction or other nucelic acid amplification tests)
41
List the 5 biochemical investigations for acute inflammation
* renal profile
* LFTs (liver function tests)
* blood glucose
* clotting tests
* lactate
42
1. Tonisilitis is usually caused by what pathogen ?
2. Name 3 infectious that tonsilitis is most commonly caused by
1. virus so it's usually viral
2. rhinovirus, coronavirus, adenovirus
43
Common bacterial pathogens related to tonsilitis include what ? what's the most common ?
beta-haemolytic and other streptococci
most common = group A beta-haemolytic streptococci
44
Most cases of acute bronchitis are due to what ?
viral infections
45
What are the diseases to do with the complement deficiency of early C components C1, C4, C2 ?
* systemic lupus erythematosus (SLE)
* glomerulonephritis
* polymyositis
46
5 steps of the activation of the inflammatory process ?
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
47
activation of the inflammatory process:
Tissue damage = detection of what ?
PAMPs/DAMPS
48
activation of the inflammatory process:
arachidonic acid mediators = activation of ...1..., formation of...2..., drugs = ...3.... ?
1. phospholipids
2. inflammatory mediators
3. NSAIDs
49
activation of the inflammatory process:
activation of macrophages = degranulation and secretion of ...1..., & ....2.....
1. histamine
2. vasodilation
50
activation of the inflammatory process:
complement activation = formation of ...1...
MAC (membrane attack complex)
51
activation of the inflammatory process:
activation of kinin system = formation of ...1... & ...2...
1. bradykinin
2. vasodilation
52
What do chemical mediators modulate ?
inflammatory response
53
6 examples of chemical mediators
* serotonin
* histamine
* complement
* bradykinin
* prostaglandin
* leukotrienes
54
Chemical mediators can either be .... or .....
endogenous, exogenous
55
If chemical mediators are endogenous where are they derived from ?
plasma proteins, leukocytes, local tissues
56
where are chemical mediators that are exogenous from ?
endotoxin from gram negative bacteria
57
what is living duration of chemical mediators ?
short-lived
58
what does every chemical mediator have ?
an inhibitor
59
what are the 6 chemical mediator groups ?
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
7. nitric oxide
60
Arachidonic acid metabolites from plasma membrane phospholipids is one of the chemical mediator
groups give 3 examples of this
* prostaglandins
* leukotrienes e.g. LTB4
* anti-inflammatory drugs (e.g. aspirin, NSAIDS, corticosteroids) working by inhibiting their synthesis
61
Key examples of vasodilation chemical mediators ?
* histamine
* prostaglandins
* bradykinin
* Nitric oxide
62
Key examples of phagocytosis chemical mediators ?
Fc (e.g. IgG antibody) & C3b = opsonins
63
Key examples of itching + pain chemical mediators ?
* bradykinin
* serotonin
* prostaglandins
64
List 5 hematological investigations for acute inflammation
* WBC count
* FBC
* CRP level (c-reactive protein level)
* ESR (erythrocyte sedimentation rate)
65
List the 2 specialised investigations for acute inflammation
* CSF analysis e.g. meningitis
* serology (lab medicine deals with detection of measurment of antibodies, antigens and other substances in the blood serum)
66
List 5 disorders of acute inflammation
* 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
1. Hereditary angioedema:
2. how rare ?
3. inheritance pattern ?
4. deficiency of ? which is what ?
5. types of oedema ?
6. family history ...?
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
2 Types of oedema in hereditary angioedema
non-itchy cutaneous angio-oedema + laryngeal and/or intestinal oedema
69
What's the disease with the complement deficiency in C3 and factor B ?
severe bacterial infections
70
Acute bronchitis can be ...1.... despite most cases being due to viral infections give examples ...2...
it is usually self-limiting
1. non-infectious
2. an inflammatory response to an irritant e.g. smoke, dust, fumes, pollutants
71
What are the symptoms of acute bronchitis due to ?
acute inflammation of the bronchial wall causing increased mucus production together with production with oedema of the bronchus
72
What are the 3 interrelated enzymatic cascade systems that produce inflammatory mediators in liver ?
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
The hallmark of a lower respiratory tract infection is the productive cough (sputum) what leads to this? [check and change?]
Acute inflammation of the bronchial wall, causes increased mucus production together with oedema of the bronchus
73
List 5 examples of some anti-inflammatories
* Aspirin / NSAIDs e.g. naproxen, ibuprofen
* antihistamines
* corticosteroids
* leukotriene antagonists e.g. montelukast
* TNF alpha antagonists e.g. infliximab
74
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
1. genetic
2. generate free radical superoxide so it can't kill the bacteria by phagocytosis
3. first year of life
4. granulomas
75
What is A1AT ?
a protease inhibitor which deactivates enzymes released from neutrophils during inflammation
76
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 ?
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
After tissue injury, next is release of chemical mediators list 4 of the chemical mediators released
1. histamine
2. complement
3. kinin (blood pressure regulation)
4. prostaglandins
78
4 sequelae of acute inflammation ?
* resolution
* suppuration (excess exudate)
* chronic inflammation (persistent causal agent)
* death
79
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)
1. short
2. regenerate
3. minimal
4. short
5. rapid
6. exudate
7. fibrin
8. thromolytic
80
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.
1. pus
2. infective
3. pyogenic
4. abscess
5. antibiotics
6. immune
81
chronic inflammation (persistent causal agent) as sequelae of acute inflammation:
* ....1....repair
* .....2.... and tissue organisation
* .....3.....tissue formation
1. fibrous
2. scarring
3. granulation
82
1. where is hypovolaemic shock often seen in ?
2. seen due to what ?
1. burns
2. insufficient blood flow or excessive injury
83
what can septic shock occur due to ?
overwhelming systemic infection resulting in vasodilation leading to hypotension
84
Obstructive shock seen in cardiac tamponade , what does the fluid do ?
fluid in the pericardium prevents venous return
85
type IV hypersensitivty reactions ...
1. mediated by ?
2. time frame ?
1. T cells
2. delayed (24 to 72 hours)
86
Type III hypersensitivity is..
1. mediated by ?
2. time frame ?
1. antigen-antibody imune complexes
2. hours to days/weeks
87
examples of type IV hypersensitivity reactions?
1. contact dermatitis
2. tuberculin skin test
88
examples of type III hypersensitivity reactions
* serum sickness
* RA
* SLE
* post-streptococcal glomerulonephritis
89
examples of Type II hypersensitivity reactions
* haemolytic disease of the newborn
* autoimmune haemolytic anaemia
* goodpasture's syndrome
90
Type II hypersensitivity :
1. mediated by ?
2. time frame ?
1. IgG or IgM antibody (cytotoxic)
2. hours to days
91
Type I hypersensitivity is :
1. mediated by ?
2. timeframe ?
1. IgE antibody
2. immediate (minutes)
92
3 examples of type I hypersensitivity reactions
* allergy
* anaphylaxis
* atopy
93
sensitisation to an allergen on re-exposure can develop ....1.... reaction
....2.... infection or long term exposure can lead to ...3.... complexes
1. hypersensitivity
2. persistent
3. antigen-antibody
94
Airway swelling in acute epiglottis results in raised ..1.., ..2... herniation / coning in acute bacterial ...3... due to obstruction of CSF channels
1. ICP
2. tonsillar
3. meningitis
95
List 6 examples of local complications
* 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
Systemic effect of shock = circulatory failure (clinical syndrome) ,
1. what is it due to ?
2. often .... ?
1. spread of microorganisms and toxins (septic shock)
2. fatal
97
List 5 acute phase proteins released from the liver
* fibrinogen
* CRP (C-reactive protein)
* alpha1 antitrypsin
* Haptoglobin
* Serum amyloid A protein
98
how does pain and loss of function combat injury ?
enforces rest, reduces chance of further traumatic damage
99
How does infiltration of inflammatory cells combat injury ?
removes pathogenic organisms, necrotic debris
100
How does vasodialtion combat injury ?
increases delivery, increases temperature
100
How does the exudation of fluid combat injury ?
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
Hallmark of acute inflammation loss of function results from what ?
loss of mobility due to oedema, pain or replacement of cells
102
Hallmark of acute inflammation heat results from what ?
vasodilation
103
Hallmark of acute inflammation swelling results from what ?
oedema, exudate due to vasodilation and increased permeability of blood vessels
104
Hallmark of acute inflammation pain results from what ?
bradykinin, prostaglandins released
105
Hallmark of acute inflammation redness 'rubor' results from what ?
vasodilation in vascular phase (more blood flow)
106
Summarise the role of neutrophils in acute inflammation
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
Toxic oxygen species is converted to hydrogen peroxide by ...1.... from neutrophil granules
...2.... - halide system -> hypochlorite
1. myeloperoxidase
2. H2O2-myeloperoxidase
107
The debris from a phagocyte are released by exocytosis, engulfed cells can be killed in one of 2 ways what are these 2 ways ?
* oxygen dependent mechanisms
* oxygen independent mechanisms
108
Oxygen dependent mechanism:
1. what's released into the phagosome ?
2. mechanism of killing known as ?
1. oxygen derived free radicals
2. oxidative burst
109
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 ?
1. enzymes
2. proteases, lipases, nucleases
3. nucleases from neutrophil granules
110
what are the 4 steps of phagocytosis ? use bacterium as an example
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
what is margination ?
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
What are the 6 steps that neutrophils infiltrate the tissue and attach to bacteria ?
1. chemotaxis
2. activation
3. margination
4. diapedesis
5. recognition attachment
6. phagocytosis
113
Chemotaxis = 1st step that neutrophils infiltrate the tissue and attach to bacteria
explain what it is ?
neutrophils attracted towards the site of injury by chemical attractants
114
activaiton = 2nd step that neutrophils infiltrate the tissue and attach to bacteria
explain what it is ?
neutrophils switch to a higher metabolic level and change shape to help them move towards the chemical attractant
115
margination = 3rd step that neutrophils infiltrate the tissue and attach to bacteria
explain what it is ?
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
diapedesis = 4th step that neutrophils infiltrate the tissue and attach to bacteria
explain what it is ?
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
recognition attachment = 5th step that neutrophils infiltrate the tissue and attach to bacteria
explain what it is ?
neutrophils recognise the bacterium via the opsonins which attract to the bacterium
neutrophils then move towards and attach to the bacterium
118
phagocytosis = 6th step that neutrophils infiltrate the tissue and attach to bacteria
explain what it is ?
process by which neutrophils engulf and destroy the bacteria
119
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.....
1. rapid response to injury
2. vascularised living
3. defensive
4. infection
5. damaged tissue
120
What are the 4 stages that acute inflammation can be broken down into ?
* 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
How do neutrophils escape from vessels ?
* relaxation of inter-endothelial cell junctions
* digestion of vascular basement membrane
* movement
121
List examples of chemotaxins in the stage of diapedesis
* C5a
* LTB4
* cytokines (endogenous)
* bacterial products (exogenous)
* clotted blood
122
What are the receptors/ chemical mediators at the diapedesis stage of neutrophil extravasation ?
* chemotaxins
* e.g. C5a, leuktriene B4, bacterial peptides
* stimulate neutrophils to migrate through the inter-endothelial cell junctions
123
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
1. integrin ligands
2. C5a, IL-1, TNF
124
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.
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
What are the 4 steps of neutrophil extravasation ?
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
what are neutrophils also known as ?
primary leukocyte = neutrophil (also known as neutrophil leukocyte, neutrophil polymorph, PMN, polymorph)
127
neutrophils are ....1... cells involved in ...2...inflammation , they are type of ....3..., first .....4.... hrs, ...5...-lived
1. wbc
2. acute
3. granulocyte
4. 6-24
5. short
128
List 4 types of exudate (fluid with high protein content e.g. acute inflammation) and an example where found ?
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
In heart failure although increased ...1... pressure the vessel is ...2... and don't leak ...3... proteins so ..4... osmotic pressure is static
1. hydrostatic
2. intact
3. plasma
4. colloid
130
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 ?
1. transudate = fluid with low protein content
2. exudate = fluid with high protein content e.g. acute inflammation
131
What are the 3 main components of inflammation ?
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
what are the 2 phases of acute inflammation ?
vascular & cellular
133
what are the changes in tissue that happen in the vascular & cellular phases of acute inflammation ?
vascular: changes in blood blow (INC blood flow) , exudation of fluid into tissues
cellular: infiltration of inflammatory cells
134
What modulates the changes in tissue of vascular & cellular phases of acute inflammation
different inflammatory mediators modulate these steps
135
Vascular phase: mechanisms of vascular leakage exudation occurs as a result of several mechanisms:
1. endothelial contraction
2. cytoskeletal reorganisation
3. direct injury
4. leukocyte-dependent injury
5. increased transcytosis
136
Exudate fluid allows what like firbin to happen ?
plasma proteins to be delivered directly to the injury site
137
What is endothelial contraction mediated by ?
histamine and leukotrienes
138
what is cytoskeletal reorganisation mediated by ?
* cytokines
* IL-1
* TNF-alpha
139
Direct injury from ...1.... or ...2.... is one mechanism of vascular leakage exudation
toxic burns , chemicals
140
leukocyte-dependent injury may happen due to what ?
toxic oxygen species or enzymes from leukocytes
141
1. what is transcytosis ?
2. mediated by what ?
1. channels across endothelial cytoplasm
2. VEGF
142
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)
1. transient
2. short
3. vasodilation
4. capillaries
5. INC
6. exudation
7. slowing
8. stasis
9. concentration
143
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
1. malaise, anorexia, nausea
2. acute
3. protein
144
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....
1. macrophages + endothelial
2. colony
3. leukocytes
4. TNF alpha
5. neutrophils
6. lymphocytes
145
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)
1. bacterial
2. pyrogenic
3. anterior
4. prostaglandins E2
