Inflammation, Inflammatory disorders, Wound healing Flashcards
Activated Hageman factor activates
Coagulation and fibrinolytic system
Complements
Kinin system
Alternative pathway of activating complements involves
Microbial products directly activate complements
Arachidonic Acid released from phospholipid cell membrane by
Phospholipase A
C1 inhibitor deficiency results in
Hereditary angioedema
C5a is
Chemotactic for PMN
Chediak-Higashi clinical
- Increase risk of pyogenic infections
- Neutropenia (Due to intramedullary death of PMN)
- Giant granules in leukocytes
- Albinism
- peripheral neuropathy
Chediak-Higashi syndrome is
AR protein trafficking defect characterized by impaired phagolysosome formation
Classic pathway of activating complements involves
C1 binds IgG or IgM that is bound to antigen
CREST is
- Calcinosis
- Raynaud phenomenon
- Esophageal dysmotility
- Sclerodactyly
- Telangiectasias of skin
CREST lab findings
Anti-centromere AB
Cu in wound healing
Cofactor for lysyl oxidase
DiGeorge clinical
- T-Cell deficiency due to lack of Thymus
- Hypocalcemia due to the lack of parathyroids
- Abdormalities of heart, great vessels and face
DiGeorge sydrome due to
22q11 microdeletion
DiGeorge sydrome is a developmental failure of
the 3rd and 4th pharyngeal pouches
Drug induced SLE lab findings
Antihistone AB
During adhesion, integrins are upregulated on leukocytes by
Cha and LTB4
E-selectin induced by
TNF and IL-1
Fibroblast growth factor role in wound healing
Important for angiogenesis
Granulomas are a collection of
Epithelioid histiocytes (macrophages with abundant pink cytoplasm) surrounded by giant cells and rim of lypmphocytes
H2O2 to HOCl
MPO
Hageman factor (Factor ΧΙΙ) is
inactive proinflammatory protein produced in liver
Hyper-IgM syndrome due to
Mutated CD40L inhibiting class switching
LAD clinical
- Delayed separation of umbilical cord
- Increase circulating PMN
- Recurrent bacterial infections that lack pus formation
latelet-derived growth factor role in wound healing
GF for endothelium, smooth muscle, and fibroblasts
Leukocyte adhesion deficiency genetics
AR defect of Integrins
O2- to H2O2
Superoxide Dimutase
O2 to O2-
Oxidative burst
NADPH oxidase
Source of CGD
P-selectin released from
Weibel-Palade bodies bediated by histamine
Scleroderma is
Autoimmune tissue damage with activation of fibroblasts and deposition of collagen
Scleroderma lab findings
anti-DNA topoisomerase 1 (Scl-70)
Sjögren lab findings
Anti-ribonucleoprotein AB (anti-SS-A/Ro and anti-SS-B/La)
Sjögren sydrome is
Autoimmune destruction of lacrimal and salivary gland
Sjögren syndrome increases risk of
B-cell (marginal zone) lymphoma
SLE clinical
- Fever and weight loss
- Malar ‘butterfly’ rash
- Arthritis
- Pleuritis and pericarditis
- Psychosis
- Renal damage
- Libman-Sacks endocarditis
- Anemia, thrombocytopenia, leukopenia
SLE lab findings
ANA (sensitive but not specific)
anti-dsDNA AB (Specific)
TGF-α role in wound repair
Epithelial and fibroblast growth factor
TGF-β role in wound repair
Fibroblast growth factor also inhibits inflammation
TH1 secrete
IL-2 (T cell growth factor and CD8 T-cell activator)
IFN-γ (macrophag activator)
TH2 secretes
- IL-4 (B-cell class switching to IgG and IgE)
- IL-5 (Eosinophil chemotaxis and activation, maturation of B cells, IgA class switching)
- IL-10 (Inhibits TH1)
TLR activation results in
upregulation of NF-κB
TLRs are activated by
Pathogen-associated molecular patterns (PAMPs)
Toll-Like receptors (TLR) are
Mediators of acute inflammation
Located on cells of innate immune system
Vit C in wound healing
Cofactor in hydroxylation of proline and lysine
What AA metabolite attracts and activates PMN
LTB4
What AA metabolite mediates Pain and Fever
PGE2
What AA metabolites mediate vasodilation and increased vascular permeability
- PGI2
- PGD2
- PGE2
What drugs cause SLE
Hydralazine
Procainamide
Isoniazid
What test is used to screen CGD
Nitroblue tetrazolium test
(remains colorless if NADPH oxidase is defective)
What type of HS is Sjögren sydnrome
4
What type of HS is SLE
2 and 3
What upregulates ICAM and VCAM
TNF and IL-1
Wiskott-Aldrich sydrome clinical
- Thrombocytopenia
- Eczema
- Recurrent infections
Wiskott-Aldrich syndrome due to
X-linked mutation of WASP
X-linked Agammaglobulinemia is
Complete lack of Ig due to disordered B-cell maturation
X-linked Agammaglobulinemia is due to
Mutated BtK
Zinc in wound healing
Cofactor for collagenase which replaces Type 3 collagen with Type 1