Blood: Haemostasis, Inflammation, Healing Flashcards
Cells in the blood and their functions
RBCs: carry oxygen - come from bone marrow stem cells
WBCs: 2 types (Neutrophils and Lymphocytes) used in the immune defence system
Platelets: Blood clotting and Inflammation
Plasma: Water, salts and proteins (Serum is blood without the coagulation factors)
Functions of blood?
Transport: moves oxygen, nutrients, hormones around body and removes waste products.
Defence: Immunity and blood clotting. Prevents excess blood loss and entry of pathogens.
Homeostasis: constant internal environment, like PH, water, temp.
What is Haemostasis?
Primary vs Secondary Haemostasis?
- Coagulation. Plug formed of platelets and fibres.
- Primary is where the platelets adhere to endothelium, activated, and then aggregate with a fibrin mesh. Secondary is the clotting cascade.
Steps in Primary Haemostasis?
- Adherence: endothelium release vWF to bind to the exposed collagen fibres. Platelets bind to the collagen/vWF receptors to activate = express Fibrinogen receptors on membrane.
- Activation: platelets bind to fibrinogen, which links many activated platelets together. Also, they release other aggregation signalling molecules to attract more platelets to the site.
- Aggregation: new platelets bind to those on the site of clot.
Steps in Secondary Haemostasis?
Tissue factors (TF) bind to F7a = activation of F10a. F10a causes Prothrombin→Thrombin. Thrombin enzyme causes Fibrinogen→Fibrin. Thrombin also activates platelet and endothelium receptors = ↑platelet aggregation and ↑vWF release; POSITIVE FEEDBACK
Fibrinolysis: What it does, and how?
Used to terminate coagulation.
tPA is used to convert Plasminogen→Plasmin, which breaks down fibrin mesh.
Haemophilia
Thrombosis
Disseminated Intravascular Coagulation (DIC)
- When clotting can’t occur due to mutations in coag factors. This can lead to excessive haemorrhage and swelling.
- Clotting in wrong place. In arteries, this can lead to an ischaemic stroke, and in veins, a DVT.
- Whole body clots, may be in response to sepsis.
Triggers and roles of acute inflammation?
Signs of acute inflammation? What causes them?
- Triggered by pathogens, irritants, trauma, foreign material. Roles include to limit spread, alert body, protect site from infection, kill dead tissue and create optimum healing conditions.
- Redness (rubor): due to ↑blood flow
Swelling (tumor): ↑fluid accumulation from increased vessel permeability
Heat (calor): ↑metabolic activity
Pain (dolor): increased pressure on nerve endings
Loss of function: due to swelling and pain
Vascular changes in acute inflammation?
Cellular changes in acute inflammation?
- Vasodilation due to histamine and serotonin release from injured cells
Increased blood flow
Increased vessel permeability due to contraction of endothelial cells - Migration and accumulation of neutrophils
Removal of pathogens, damaged/dead cells by neutrophils
Migration and accumulation of monocytes - become macrophages to release factors that promote tissue repair
Molecules involved in neutrophil recruitment
- Selectins: mediate the rolling of neutrophils and are expressed by activated endothelial. Endothelial selectins can bind to ligands on neutrophil surface = low affinity binding, disrupted by blood flow. Repetitive binding and detaching = rolling.
- Integrins: expressed on neutrophils with a low affinity configuration. Activated endothelium produce CHEMOKINES to bind to neutrophils receptors = activation of integrins. They now have a high affinity configuration and can now bind to the ligands on the endothelium = firm grip.
- Neutrophil transmigration: neutrophils move through endothelial spaces. They’re attracted to the inflamed site by chemoattractants; Chemotaxis.
What are the 3 Outcomes of acute inflammation
- Complete resolution of the affected tissue.
- Lost tissue replaced by connective tissue - scarring.
- If no termination occurs, it could lead to chronic inflammation.
What is chronic inflammation?
How does it compare with acute inflammation?
- Prolonged response that can come after acute inflammation due to persistent infection or autoimmunity.
- Lasts months/years, has a slow onset, uses lymphocytes/fibroblasts/ macrophages. Also, it leads to severe tissue destruction, fibrosis, necrosis.
What cells are involved in chronic inflammation? What are their roles?
Macrophages - destroy dead cells and activate other cells by secreting inflammatory cytokines.
Lymphocytes - T cells produce cytokines fro macrophage activation. B cells form plasma cells to produce antibodies.
Eosinophils: destroy parasites
Mast cells
Neutrophils
What are the 4 main types of chronic inflammation?
- Non-specific: develops when acute inflammation fails to remove the pathogen. This leads to tissue destruction, like gastric ulcers.
- Autoimmune: due to immune response to self-antigens. No acute inflammation before. Tissue damage occurs over time e.g. R.Arthritis.
- Chronic Suppurative: starts with acute inflammation, and pus accumulates to form an abscess.
- Chronic Granulomatous: occurs when the agent can’t be removed. Granuloma’s form to isolate the agent and prevent spread. Have a cluster of macrophages in the centre, a rim of lymphocytes, fibroblasts, and connective tissue. Inside is a multinucleate giant cell and central necrotic area.
What is tissue healing and repair?
What is primary and secondary healing/intention?
- Tissue regeneration or replacement.
- Primary intention is where injury is only to the epithelial layer, so complete healing can occur e.g. small incision. Secondary intention is where there’s lots more tissue damage/loss, so fibrosis occurs e.g. large wounds, abscess removal.
