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Pathology > Chapter 2 ( Inflammation , Wond Healing ) > Flashcards

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
Q

CGD patients susceptible to what organisms ?

A 
Catalase positive organisms : 
Staph aureus 
Pseudomonas Cepacia 
Serratia marcocescens 
Nocardia 
Aspergillus
26
Q

What organism do MPO patients is most susceptible to ?

A

Candida infections

27
Q

By which enzymes does oxygen independent killing occur ?

A

Enzymes present in leukocyte secondary granules as :
1- Lysozyme in macrophages
2-Major basic proteins in eosinophils

28
Q

Different outcomes of management of macrophages of inflammatory process ?

A

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
Q

Stimuli for chronic inflammation ?

A 
Persistent infection 
Infection with viruses , mycobacteria , parasites , fungi 
Autoimmune disease 
Foreign material 
Some cancers
30
Q

T cell receptor complex components and function ?

A

TCR and CD3

Used by T cells for antigen surveillance

31
Q

2nd activation signal for CD4 helper T cells ?

A

B7 on APC binds CD28 on CD4 helper T cells

32
Q

Cytokines secreted by activated CD4 helper T cells ? Their functions ?

A

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
Q

2nd activation signal of CD8 cytotoxic T cells ?

A

IL2 from CD4 helper TH1 cell

34
Q

Activation of B cells ?

A

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
Q

Granuloma structure ?

A

Epithelioid histiocytes
Giant cells
Rim of lymphocytes

36
Q

Causes of noncaseating granuloma ?

A 
Foreign material
Sarcoidosis 
Beryllium exposure 
Crohn disease 
Cat scratch disease
37
Q

Causes pf caseating granuloma ?

A 
TB (AFB stain)
Fungal infections (GMS stain)
38
Q

DiGeroge syndrome defect and presentation ?

A

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
Q

SCID etiology ? Susceptible to which organisms ? Ttt ?

A

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
Q

Aggamaglobulinemia defect ? Presentation ?

A 
X linked 
Mutated Bruton tyrosine kinase 
Presents after 6 months of life with :
Recurrent bacterial 
Enterovirus ( polio and coxsakievirus )
Giardia Lamblia infections
41
Q

Most common immunoglobulin deficiency ?

A

IgA deficiency

Associated with increased risk for mucosal infections especially viral

42
Q

Hyper IgM syndrome defect ? Characteristics ?

A

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
Q

Wiskott-Aldrich syndrome defect ? Presentation ?

A 
X linked
Mutation in the WASP gene 
Presents by :
1- Thrombocytopenia 
2- Eczema 
3- recurrent infections
44
Q

C5-C9 deficiency increase risk for ?

A

Neisseria infections ( gonorrhoeae , meningitidis )

45
Q

C1 inhibitor deficiency results in ?

A

Hereditary angioedema ( skin and mucosal surfaces )

46
Q

SLE mechanism and clinical features ?

A 
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
Q

Antibodies of SLE ?

A

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
Q

Causes of drug induced lupus ?

A

Hydralazine
Procainamide
Isoniazid

49
Q

Most common feature of antiphospholipid syndrome ?

A 
Venous and arterial thrombosis : 
1-DVT
2-Budd chiari syndrome 
3-Recurrent pregnancy loss 
4-Stroke
50
Q

Sjorgen syndrome mechanism and clinical features ? Antibodies ? Increased risk for what ?

A 
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
Q

Antibody of localized scleroderma ?

A

Antibody to DNA topoisomerase ll

52
Q

CREST syndrome ?

A 
Calcinosis / anti Centromere antibodies 
Raynaud phenomenon 
Esophageal dismotility
Sclerodactyly 
Telangiectasias of skin
53
Q

Antibody of mixed connective tissue disease ?

A

Antibodies of U1 ribonucleoprotein

54
Q

Mechanism of scleroderma ?

A

Activation of fibroblasts and deposition of collagen ( fibrosis )

55
Q

Labile tissues and site of their stem cells ?

A

1- small and large bowel ( in mucosal crypts )
2- skin ( basal layer )
3- bone marrow ( hematopoietic stem cells )

56
Q

Granulation tissue of initial phase of repair components?

A

1- Fibroblasts that deposit type lll collagen
2- capillaries
3- myofibroblasts that contract the wound

57
Q

Last step of scar formation ? Responsible enzyme ?

A

Type lll collagen is replaced with type l collagen

By Collagenase enzyme that requires Zinc as cofactor

58
Q

Mechanism of tissue repair and regeneration ? Examples ?

A

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
Q

Causes of delayed wound healing ?

A 
Infection 
Vit C , copper , zinc deficiency 
Foreign body 
Ischemia 
DM
Malnutrition

Pathology (18 decks)

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