Case 1 Flashcards
(102 cards)
Mast cells release..
Histamine
Factors responsible for angiogenesis:
VEGF
FGF-2
PDGF
First stage of wound healing
Inflammation
Role of macrophages in wound healing
Removal of tissue debris Angiogenesis Antimicrobial Chemotaxis Proliferation of fibroblasts and keratinocytes Deposition and remodelling of ECM
During wound healing, neutrophils are replaced with macrophages after…
48-96hrs
First intention wound healing
Small scab consisting of: fibrin clot, neutrophils, and macrophages
Growth factor secreted which brings edges of wound together.
Sutures for first intention wound are removed after…
1 week
Second intention wound healing
Large scab consisting of: fibrin clot, neutrophils and macrophages.
More granulation tissue formed.
Wound edges brought together by contraction of myofibrils.
Increased risk of infection - requires regular cleaning.
Broader scar formed.
PGE2 and Pain
Sensitises A-delta and C nociceptive neurones to serotonin, substance P and Bradykinin
Stimulates chemotaxis.
How do pyrogens cause an increase in body temperature?
Cause hypothalamic PGHS2 to generate PGE2
MOA of Ibuprofen
Competitive reversible inhibition of COX1 domain of PGHS-1 and PGHS-2
MOA of aspirin
Acetylation of COX domain of PGHS. Causes irreversible inhibition.
Pathophysiological effects of PGHS-1
Chronic pain
Hypertension
Pathophysiological effects of PGHS-2
Inflammation
Chronic pain
Why does ibuprofen (and other NSAIDs) cause gastric ulceration?
Inhibition of COX domain of PGHS. Inhibits synthesis of prostaglandins which normally inhibit gastric secretion and protect the mucosa.
Primary Haemostasis
Exposed collagen causes activation of integrin receptors. Platelet aggregation to each other and the damaged vessel wall via integrins.
This requires Von Willibrand Factor.
Formation of a platelet plug which stops blood flow from minor wounds and provides a surface for strengthening reactions to occur on.
Extrinsic Pathway of Secondary Haemostasis
Tissue damage activates tissue factor III
TF III forms an active complex with VII (VIIa:III) - Ca2+ dependent
VIIa:III activates TF X (Xa)
Intrinsic pathway of Secondary Haemostasis
Damage to a vessel causes activation of TF XII (XIIa) - requires HMW-K and kallikrein.
XIIa converts prekallikrein to kallikrein (stimulating more XII activation)
XIIa also activates XI (XIa)
XIa activates IX (IXa)
IXa activates X (Xa)
Final Common pathway in Secondary Haemostasis
TF X was activated in extrinsic and intrinsic pathways.
Xa converts Prothombin to thrombin (requires Ca2+, Va and platelet surface)
Thrombin activates TF V and VIII (stimulating more thrombin production)
Thrombin converts fibrinogen to fibrin and activates XIII.
XIIIa stabilises fibrin resulting in clot formation
Haemophilia A
TF VIII deficiency
Haemophilia B
TF IX deficiency
Haemophilia C
TF XI deficiency
Von Willibrand’s Disease
I - little vWF
II - poor functioning vWF
III - no vWF
Thrombocytopathia
Reduction in platelets