Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

mechanism of disease > Real Inflammation > Flashcards

Real Inflammation Flashcards

(118 cards)

Start Studying
1
Q

Inflammation

A

Response of living vascularized tissue to injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Goal of inflammation

A

Remove damaged, necrotic tissues and foreign invaders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Repair

A

Injured tissue is replaced through

  • regeneration of native parenchyma tissue
  • by filling of defect with fibrous tissue
  • both
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cardinal signs of inflammation

A

Rubor -redness
Dolor -pain
Calor - fever
Tumor - swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Fifth signs of inflammation

A

Loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

2 types of inflammation

A

Acute and chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute inflammation

A

Rapid onset
Short duration ( hours to days )
Exudation of fluid and plasma proteins leading to edema
Emigration of leukocytes , mostly neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

3 characteristics of acute inflammation

A

> alteration in vascular caliber leading to increased blood flow

> structural changes in micro vascular use to allow plasma cells to get into tissues

> emigration of leukocytes to site of injury , accumulation and activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Stimuli of acute inflammation

A

Infections

Tissue necrosis ( ischemia , trauma, mechanical injury )

Foreign Bodies

Immune reaction like in hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Changes in vascular flow and caliber

A

Transient constriction for few seconds

Vasodilation ( arterioles and then to the capillaries ) => NO and histamine

Increased permeability

Stasis of blood and more viscous blood

Leukocytes adhesion to endothelium and migrations through the wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Increased vascular permeability

A

Contraction of endothelial cells

Increased interendothelial cells (histamine, bradykinin, leukotrienes, neuropeptide substance b)

EnDothelial injury

Endothelial cell necrosis and detachment

Transcytosis => increased transport of fluids and proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Responses of lymphatic vessels

A

Lymph flow increased to drain edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How would you have lymphangitis or lymphadenitis in acute inflammation

A

Leukocytes , debris and microbes find their way into the lymph during drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Lymphangitis

A

Inflammation of the lymphatic channels because of infection distal to channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Lymphadenitis

A

Inflammation of the lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Recruitment of leukocytes to site of infections

A

Margination
Rolling
Adhesion to endothelium

Migration across endothelium and vessel wall (diapedesis)

Migration into tissue towards chemotactic stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Rolling of leukocytes mediators ( receptors on left, ligand on the right )

A

L-selecting (leukocyte ) —- Glycam-1, CD34 (endothelium)

E-selectin (endothelium ) —- sialyl-lewis X modified protein (leukocytes )

P-selecting (platelet and endothelium ) —- sialyl-lewis X modified protein (leukocytes )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Adhesion of leukocytes mediators (ligand on the right )

A

VLA-4 integrin (leukocyte ) —— VCAM-1 (endothelium)

LFA-1 integrin (leukocyte ) —— ICAM-1 (endothelium)

MAC-1 integrin (leukocyte ) —— ICAM-1 (endothelium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

VLA-4

A

Very late antigen 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

LFA-1

A

Lymphocyte function associated antigen 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

VCAM 1

A

Vascular cell adhesion molecule 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ICAM 1

A

Intercellular adhesion molecule I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Leukocytes migration through endothelium mediators (ligand on right )

A

PECAM-1 CD31 (endothelium) ——- ligand (leukocyte )

Collagenase (break down basement membrane )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

PECAM1 h

A

Platelet endothelial cell adhesion molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Chemotaxis
Locomotion oriented along a chemical gradient produced by chemoattractants
26
Exogenous chemoattractants
Bacterial products ( peptides with n-formylmethionine) , lipids
27
Endogenous chemoattractants
Cytokines ( IL8) Complement system C5a Arachidonic acid metabolites like leukotrienes B4
28
Chemotaxis process
Chemotactic agent binds G protein receptor on leukocyte surface Signal initiated Secondary message which increases calcium and activate the Rac/Rho/ cdc42 Polymerizatioj of actin induced which increases its quantity at edge of cell Leukocyte moved by filopodia towards stimuli
29
Dominant leukocytes during first 6 to 24 hours of acute inflammation
Neutrophils
30
Leukocyte that replaced neutrophils after 24 hours to 48 hours
Monocytes
31
Who survive longer neutrophils or monocytesu
Monocytes
32
Cellular infiltration that do not have same infiltration pattern in acute inflammation
Pseudomonas bacteria - neutrophils dominate for several days Viral infection - lymphocytes may Some hypersensitivity rxns- eosinophils dominant
33
Recognition of microbes and dead tissues by
Toll like receptors G protein coupled receptors on macrophages, neutrophils and other leukocytes Receptors for opsinins Receptors for cytokines
34
Toll like receptors recognize
Bacteria lipopolysaccharide (LPS) Bacterial Proteoglycans and lipids Unmethylated CpG nucleotides dsDNA viral
35
G protein coupled receptors on macrophages, neutrophils and other leukocytes recognize...
Small bacterial peptide with n formylmethionyl Chemokines Product of complement such as c5a Lipid mediators PGs Leukotrienes
36
Receptors for opsinins recognize
Antibodies Complement proteins Lectins
37
Opsonization
Coating of particle to make it more disgestable through phagocytosis
38
Receptors for cytokines recognize
Cytokines (inf-y)
39
Removal of offending agents in acute inflammation
``` Phagocytosis : Recognition and attachment Particle engulfment Vacuole formation with particle inside Killing and degradation of particle ```
40
In acute inflammation, how is engulfed particle killed
ROS (superoxide ion) Reactive nitrogen species ( NO, peroxynitrite) Enzymes like elastase Microbicidal granules (defensins, lactoferrin, lysozyme, Cathelicidins)
41
What leukocytes when activated promote proliferation of endothelial cells and fibroblasts , and synthesis of collagen
Macrophages
42
Leukocytes induced injury
Collateral damage as part of normal defense reaction In appropriate target of Inflammatory response
43
Leukocyte induced injury examples
Acute respiratory distress syndrome with neutrophils Acute transplant rejection by lymphocytes antibodies and complement Asthma by eosinophils IGE antibodies Glomerulonephritis By neutrophils monocytes antibodies complement Septic shock by cytokines Like abscess by neutrophils and bacteria Arthritis by lymphocytes macrophages and antibodies Atherosclerosis by macrophages and lymphocytes Chronic transplants rejection by lymphocytes and cytokines
44
Leukocytes genetic defects
Leukocyte adhesion deficiency 1 Leukocyte adhesion deficiency 2 Chronic granulomatous disease=> decreased oxidative burst X linked => phagocyte oxidase membrane component Autosomal recessive => phagocyte oxidase cytoplasmic component MPO deficiency => decreased microbial killing because deficient MPO Chediak higashi syndrome
45
Leukocyte adhesion deficiency 1
Mutation in beta chain CD11/CD18 integrans - defective leucocyte adhésion
45
Genetic defect in leukocytes function
``` Leukocytes adhesion deficiency 1 leukocyte adhesion deficiency 2 Chronic granulomatosis disease X linked Autosomal recessive MPO Deficiency Chediak higashi syndrome ```
46
Leukocyte adhesion deficiency 2
Mutation in fucosyl transferase fr synthesis of sialylated oligosaccharadise - defective leucocyte adhésion
47
Chronic granulomatosis disease X linked
Decreased oxidative burst due to Phagocytes oxidase (membrane components)
48
Chronic granulomatosis disease Autosomal recessive
Decreased oxidative burst due to phagocyte oxidase but cytoplasmic component
49
MPO deficiency
Defect in macrophages causing decreased microbial clearance
50
Chediak higashi syndrome
Decreased leukocyte function due to mutations | Affect protein involved involved in lysosomal membrane traffic
51
Acquired defects in leukocyte function
Bone marrow suppression ( tumors , radiation, chemotherapy) - production of leukocyte Diabetes, malignancy, sepsis , chronic dialysis - adhesion, chemotaxis Leukemia, anemia, sepsis, diabetes, malnutrition - phagocytosis , microbicidal activity
52
Mediators of inflammation for termination
Produced in rapid bursts when stimuli present Short half lives Degraded after release
54
Cytokines released by macrophages for anti inflammation response
IL 10 | TGF BETA
55
Anti inflammatory lipid mediators
Resolvins | Protectins
56
Neural impulses in antiinflammation
Cholinergic discharge | Inhibit production of TNF in macrophages
57
Types of mediators of inflammation
Cell derived mediators Plasma protein derived mediators
58
Cell derived mediators of acute inflammation
``` Platelets Neutrophils Monocyte macrophages Mast cells Mesenchymal cells ( endothelium, smooth muscle , fibroblasts ) Ahh ```
59
Plasma protein derived mediators
Complement proteins Kinins Present in blood as inactive precursors
60
Cell derived mediators that release HISTAMINE
Mast cells Basophils Platelets
61
Histamine action
Vasodilation Increased permeability Endothelial activation
62
Cell derived mediators that release serotonin
Platelets
63
Role of serotonin
Vasodilation | Increased permeability
64
Cell derived mediators that release prostaglandins
Mast cell , leukocyte
65
Prostaglandins role
Vasodilation Pain Fever
66
Cell derived mediators that release leukotriene
Mast cell | Leukocytes
67
Leukotriene action
Increased vascular permeability Chemotaxis Leukocyte adhesion And Activation
68
Cell derived mediators that release platelet activating factors
Leukocytes | Mast cells
69
Platelet activating factor role
``` Vasodilation Increased vascular permeability Leukocyte adhesion Chemotaxis Degranulation Oxidative burst ```
70
Cell derived mediators that release ROS
Leukocyte
71
ROS role
Killing of microbes | Tissue damage
72
Cell derived mediators that release nitric oxide
Endothelium | Macrophages
73
Nitric oxide role
Vascular smooth muscle relaxation | Killing of microbes
74
Cell derived mediators that release chemokines
Leukocytes | Activated macrophages
75
Chemokines roles
Chemotaxis | Leukocytes activation
76
Cell derived mediators that release cytokines ( TNF, IL1)
Macrophages Endothelial cells Mast cells
77
Cytokines roles ( TNF , IL1)
Local endothelial activation with expression of adhesion molecule ``` Fever Pain Anorexia Hypotension Decrease vascular resistance ```
78
Fibroblast effects of acute inflammation
``` Increased : Proliferation of fibroblasts Collagen synthesis Collagenase Protease PGE synthesis ```
79
Cell derived mediators that release neuropeptides ( substance P and neurokinin A)
Sensory nerves | Various leukocytes
80
Role of neuropeptides
Initiation and propagation of inflammatory response Increase vascular permeability Pain
81
Plasma protein derived mediators that release complement products (C5a, C3a, C4a)
Plasma produced in liver
82
Complement products role
Leucocyte chemotaxis and activation Vasodilation by mast cell stimulation
83
Plasma protein derived mediators that release kinins
Plasma produced by liver
84
Kinin role
Increased vascular permeability Smooth muscle contraction Vasodilation Pain
85
Proteases activated during coagulation
Plasma
86
Proteases action
Endothelial activation | Leukocyte recruitment
87
Classical complement pathway
C1 —> activated C1 Activated C1 —> C4bC2b C4bC2b —C3 convertase —> C4bC2bC3b C4bC2bC3b —C5 convertase—> C5-9 MAC complex
88
Lectin pathway
C1 —mannose binding lectin —> activated C1 Activated C1 —> C4bC2b C4bC2b —C3 convertase —> C4bC2bC3b C4bC2bC3b —C5 convertase—> C5-9 MAC complex
89
Alternative pathway
C3 —> C3b | C3b — factor B and D —> C3bBb —> C3bBb3b —> C5 convertase—> C5-9 MAC complex
90
Fate of complement activation
Destruction of microbe by leukocytes (C5a, C3a) Phagocytosis of microbe (C3b) Mac complex lysis of microbe
91
Outcomes of chronic inflammation
Complete resolution Healing by connective tissue (fibrosis ) Progression to chronic inflammation
92
Morphology pattern of acute inflammation
Dilation small blood vessels Slowing of blood flow Accumulation of leukocytes in extra vascular tissue Accumulation of fluid in extra vascular tissue
93
Special morphological features of acute inflammation
``` Serous inflammation Fibrinous inflammation Suppurative or purulent inflammation Abscess Ulcers ```
94
Serous inflammation
Outpouring of thin fluid ( effusion) that may be derived from plasma or from secretions of mesothelioma cells lining serous cavities ( peritoneal , pleural , pericardial )
95
Example of serous inflammation
Skin blister
96
Fibrinous inflammation
Due to very increase in vascular permeability Large molecule like fibrinogen pass vascular barrier Fibrin deposited in extra cellular space Occurs in large vascular leaks or in presence of procoagulant stimulus Found in body cavities that
97
Fibrinous inflammation histology
Fibrin -> eosinophilic mesh work of threads or amorphous coagulum
98
Fibrinous exudate removal
Fibrin removed by Fibrinolysis | Other debris by macrophages s
99
What happens if fibrin not removed
Stimulate ingrowth of fibroblast | Leads to scarring
100
Organization of fibrin
Conversion of fibrin to scar tissue
101
Suppurative or purulent inflammation
Production of large amount of pus or purulent exudate | Plus contains neutrophils, nécrose cells , edema fluid
102
Pyogenic bacteria
Bacteria that cause suppurative inflammation with formation of pus
103
Abscesses
Localized collection of purulent inflammatory tissue due to suppuration buried in tissue Due to deep seeding of bacteria into tissue
104
Abscess histology
Central region with mass of necrotic leukocytes and tissue cells Some of preserved neutrophils around necrosis Around it , vascular dilation parenchymal and fibroblastic proliferation occur
105
Fate of abscess
Walled off | Replaced by connective tissue
106
Ulcers
Local defect, excavation of surface of an organ or tissue Produced by shedding of inflammatory necrotic tissue Exist when tissue necrosis and resultant inflammation occur on tissues surface or near it
107
Most common site of ulcers
Mucosa of the mouth, stomach, intestines , genitourinary tract Skin and subcutaneous tissue of lower extremeties in older persons
108
Chronic inflammation
May follow acute inflammation or insidious from onset Longer duration (weeks or months) with active inflammation, tissue destruction, attempts at repair
109
Main factors of chronic inflammation
Lymphocytes and macrophages Proliferation of blood vessels Fibrosis Tissue destruction
110
Conditions with insidious onset of chronic inflammation
Rheumatoid arthritis Atherosclerosis Tuberculosis Pulmonary fibrosis
111
Causes of chronic inflammation
Persistent infections of difficult microorganism to eradicate Immune mediated inflammatory disease ( autoimmune disease , unregulated immune response against microbes , response against common substances) Prolonged exposure to potentially toxic agents Endogenous ( toxic lipid) , exogenous ( silica)
112
Morphology of chronic inflammation
Infiltration: mononuclear ( macrophages , lymphocytes ) plasma cells ( eosinophilia and mast cells ) Tissue destruction ( persistent offending agent or inflammatory cells ) Attempts at healing by connective tissue ( fibrosis ) Proliferation of small blood vessels by angiogenesis
113
Role of macrophages in chronic inflammation
``` Help in inflammation and tissue injury : ROS and NOS Proteases Cytokines , chemokines Coagulation factors AA metabolites ``` ``` Repair : Growth factors Fibrogenic cytokines Angiogenic factors Remodeling collagenesis ```
114
Granulomatois inflammation
Distinctive pattern of chronic i Inflammation Formation of granulomas in inflammation ( cellular attempt to contain offending agent difficult to eradicate) Strong activation of T lymphocytes -> macrophages activation
115
Main disease with granulmatois inflammation
Tuberculosis ``` Sarcoidosis Leprosy Syphilis Mycotic infections Irritant lipids Autoimmune disorders ```
116
Systemic effect of inflammation
``` Acute phase response : Fever High acute phase proteins ( C reactive protein, fibrinogen, serum) Leukocytosis ( neutrophilia, lymphocytes is, eosinophilia) Leukopenia ( typhoid fever, viruses, rickettsia, protozoa, TB) High pulse High blood pressure Decreased sweating Rigors Chills Anorexia Somnolence Malaise Disseminated intravascular coagulation CDV failure Metabolic disturbance Septic shock ```
117
Consequence of defective inflammation
Increased infection | delayed wound healing
118
Consequence of excessive inflammation
``` Allergies Autoimmunity Atherosclerosis IHD Neurodégénérative disease like alzheimer ```

mechanism of disease (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions