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Chapter 2 ( Inflammation , Wond Healing ) Flashcards

1
Q

Innate immunity ?

A

Epithelium
Mucous layer
Complement system
Cells : mast , macrophages , neutrophils … etc

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2
Q

Mediators of acute inflammation ?

A 
Toll like receptors 
Arachidonic acid metabolites 
Mast cells 
Complement 
Hageman factor (factor Xll)
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3
Q

Toll like receptors activated by what ? Example ?

A

Pathogen associated molecular patterns
CD14 ( coreceptor for TLR4 ) on macrophages recognizes Lipopolysaccharide (PAMP) on the outer membrane of gram negative bacteria

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4
Q

Mechanism of TLR ?

A

Upregulation of NF-kB that activate immune response genes leading to production of multiple immune mediators

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5
Q

Enzyme that produce prostaglandins ? Types and their functions ?

A

Cyclooxygenase
PGI2 , PGD2 , PGE2 : vasodilatation and increased vascular permeability
PGE2 also mediates pain and fever

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6
Q

Enzyme that produces leukotriens ? Types and functions ?

A

5-lipoxygenase
LTB4 : attracts and activates neutrophils
LTC4 , LTD4 , LTE4 : vasoconstriction , bronchospasm , increase vascular permeability

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7
Q

Mediators that attract and activates neutrophils ?

A

LTB4
C5a
IL8
Bacterial products

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8
Q

Methods of activation of mast cells ?

A

Tissue trauma
C3a , C5a
Cross liking of cell surface IgE by antigen

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9
Q

Pathways of activating complement ?

A

1- Classical pathway : C1 binds IgG or IgM thats bound to antigen
2- Alternative pathway : by microbial products
3- Mannose binding lectin pathway : MBL binds to mannose on microorganisms and activates complement

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10
Q

C3b

A

Opsonin for phagocytosis

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11
Q

MAC

A

Lyses microbes by crating a hole in the cell membrane

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12
Q

Actions of Hageman factor ?

A

1- activates coagulation and fibrinolytic systems
2- activates complement
3- activates kinin system

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13
Q

Mediators of pain ?

A

PE2

Bradykinin

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14
Q

How the Hageman factor is activated ?

A

By exposure to subendothelial or tissue collagen

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15
Q

Mechanism of fever in acute inflammation ?

A

Pyrogens ( LPS of bacteria ) causes macrophages to release IL1 and TNF which increase cycloxygenase activity in perivascular cells of the hypothalamus , increased PGE2 raises temperature set point .

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16
Q

Mechanism of rolling in acute inflammation ?

A

Selectins bind Sialyl Lewis X on leukocytes .

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17
Q

Types of selectins ?

A

P selectin from Weibel Palade bodies mediated by Histamin

E selectin induced by TNF and IL-1

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18
Q

Mechanism of adhesion in acute inflammation ?

A

Interaction between Cellular adhesion molecules ( ICAM ,VCAM ) and Integrins results in firm adhesion of the leucocytes to the vessel wall

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19
Q

What upregulates cellular adhesion molecules on the endothelium ?

A

TNF

IL-1

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20
Q

What upregulates integrins on leucocytes ?

A

C5a

LTB4

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21
Q

Leucocyte adhesion deficiency defect and presentation ?

A

Defect of integrins ( CD18 subunit )
Presentation :
Delayed separation of the umbilical cord
Increased circulating neutrophils
Recurrent bacterial infections that lack pus formation

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22
Q

Opsonins that enhance phagocytosis ?

A

IgG

C3b

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23
Q

Chediak - Higashi syndrome defect and clinical features ?

A 
A protein trafficking defect characterized by impaired phagolysosome formation 
Clinical presentation : 
1- increased risk of pyogenic infection 
2- neutropenia 
3- Giant granules in leucocytes 
4- defective primary hemostasis 
5- Albinism 
6- Peripheral neuropathy
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24
Q

What destroys phagocytosed microbes in the phagolysosomee ?

A

HOCl from H2O2 ( by Myeloperoxidase )

25
CGD patients susceptible to what organisms ?
``` Catalase positive organisms : Staph aureus Pseudomonas Cepacia Serratia marcocescens Nocardia Aspergillus ```
26
What organism do MPO patients is most susceptible to ?
Candida infections
27
By which enzymes does oxygen independent killing occur ?
Enzymes present in leukocyte secondary granules as : 1- Lysozyme in macrophages 2-Major basic proteins in eosinophils
28
Different outcomes of management of macrophages of inflammatory process ?
1- resolution and healing : by anti - inflammatory cytokines ( IL-10 , TGF-beta ) 2- continued acute inflammation : IL8 recruites more neutrophils 3- abscess : by fibrogenic growth factors and cytokines 4- chronic inflammation : macrophages present antigen to activate CD4 helper T cells , which secrete cytokines that promote chronic inflammation
29
Stimuli for chronic inflammation ?
``` Persistent infection Infection with viruses , mycobacteria , parasites , fungi Autoimmune disease Foreign material Some cancers ```
30
T cell receptor complex components and function ?
TCR and CD3 | Used by T cells for antigen surveillance
31
2nd activation signal for CD4 helper T cells ?
B7 on APC binds CD28 on CD4 helper T cells
32
Cytokines secreted by activated CD4 helper T cells ? Their functions ?
1- TH1 subset secrets INF-gamma : Activates macrophages Promotes B cells switching from IgM to IgG Promote TH1 phenotype and inhibit TH2 phenotype IL2 : T cell growth factor and CD8 T cell activator 2- TH2 subset secrets IL4 , IL13 : facilitates B cells switching to IgE IL5 : eosinophils chemotaxis and activation , B cells switching to IgA IL10 : inhibits TH1 phenotype
33
2nd activation signal of CD8 cytotoxic T cells ?
IL2 from CD4 helper TH1 cell
34
Activation of B cells ?
1- antigen binds to IgM or IgD resulting in B cell maturation to IgM- or IgD secreting plasma cells 2- CD40 receptor on B cells bind CD40 L on helper T cells providing 2nd activation signal
35
Granuloma structure ?
Epithelioid histiocytes Giant cells Rim of lymphocytes
36
Causes of noncaseating granuloma ?
``` Foreign material Sarcoidosis Beryllium exposure Crohn disease Cat scratch disease ```
37
Causes pf caseating granuloma ?
``` TB (AFB stain) Fungal infections (GMS stain) ```
38
DiGeroge syndrome defect and presentation ?
Developmental failure of the third and fourth pharyngeal pouches due to 22q11 microdeletion Presents with : T cell deficiency ( absent thymus ) Hypocalcemia ( absent parathyroid ) Abnormalities of the heart , great vessels , face
39
SCID etiology ? Susceptible to which organisms ? Ttt ?
Etiology : 1- Cytokine receptor defect 2- Adenosine deaminase deficiency 3- MHC ll deficiency Susceptible to : fungal , viral , bacterial , protozoal , opportunistic infections and live vaccines Ttt : sterile isolation , stem cell transplantation
40
Aggamaglobulinemia defect ? Presentation ?
``` X linked Mutated Bruton tyrosine kinase Presents after 6 months of life with : Recurrent bacterial Enterovirus ( polio and coxsakievirus ) Giardia Lamblia infections ```
41
Most common immunoglobulin deficiency ?
IgA deficiency | Associated with increased risk for mucosal infections especially viral
42
Hyper IgM syndrome defect ? Characteristics ?
Mutated CD40 L on helper T cells or mutated CD40 receptor on B cells High IgM and Low Ig A,G,E Recurrent pyogenic infections especially at mucosal sites
43
Wiskott-Aldrich syndrome defect ? Presentation ?
``` X linked Mutation in the WASP gene Presents by : 1- Thrombocytopenia 2- Eczema 3- recurrent infections ```
44
C5-C9 deficiency increase risk for ?
Neisseria infections ( gonorrhoeae , meningitidis )
45
C1 inhibitor deficiency results in ?
Hereditary angioedema ( skin and mucosal surfaces )
46
SLE mechanism and clinical features ?
``` Type ll and lll hypersensitivity 1- fever and weight loss 2- malar butterfly rash 3- arthritis 4- pleuritis and pericarditis 5- cns psychosis 6- renal damage ( diffuse proliferative glomerulonephritis ) 7- pancarditis ( Libman-sacks endocarditis ) 8- pancytopenia ```
47
Antibodies of SLE ?
1-ANA ( sensitive but not specific ) 2-Anti daDNA antibodies ( highly sensitive ) 3-Antihistone antibodies ( drug induced SLE ) 4-Anticardiolipin and lupus anticoagulant ( antiphospholipid antibody syndrome )
48
Causes of drug induced lupus ?
Hydralazine Procainamide Isoniazid
49
Most common feature of antiphospholipid syndrome ?
``` Venous and arterial thrombosis : 1-DVT 2-Budd chiari syndrome 3-Recurrent pregnancy loss 4-Stroke ```
50
Sjorgen syndrome mechanism and clinical features ? Antibodies ? Increased risk for what ?
``` Type lV hypersensitivity 1- dry eye 2-dry mouth 3- recurrent dental carries ANA and antiribonucleoprotein antibodies ( anti Ro - anti La ) Increase risk for B cell lymphoma ```
51
Antibody of localized scleroderma ?
Antibody to DNA topoisomerase ll
52
CREST syndrome ?
``` Calcinosis / anti Centromere antibodies Raynaud phenomenon Esophageal dismotility Sclerodactyly Telangiectasias of skin ```
53
Antibody of mixed connective tissue disease ?
Antibodies of U1 ribonucleoprotein
54
Mechanism of scleroderma ?
Activation of fibroblasts and deposition of collagen ( fibrosis )
55
Labile tissues and site of their stem cells ?
1- small and large bowel ( in mucosal crypts ) 2- skin ( basal layer ) 3- bone marrow ( hematopoietic stem cells )
56
Granulation tissue of initial phase of repair components?
1- Fibroblasts that deposit type lll collagen 2- capillaries 3- myofibroblasts that contract the wound
57
Last step of scar formation ? Responsible enzyme ?
Type lll collagen is replaced with type l collagen | By Collagenase enzyme that requires Zinc as cofactor
58
Mechanism of tissue repair and regeneration ? Examples ?
Mediated by paracrine signaling via growth factors : 1- TGF-alpha : epithelia and fibroblast growth factor 2- TGF-beta : fibroblast growth factor and inhibits inflammation 3- platelet derived growth factor : for smooth muscles , endothelium , fibroblasts 4- fibroblast growth factor : for angiogenesis and skeletal development 5- vascular endothelium growth factor : for angiogenesis
59
Causes of delayed wound healing ?
``` Infection Vit C , copper , zinc deficiency Foreign body Ischemia DM Malnutrition ```

Pathology (18 decks)

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