WEEK 5 Flashcards
All the cells of the immune response come from the same progenitor cell. What is said cell called?
Hematopoetic stem cell
Name, and describe, the various stages of the three different types of immune response elicited by the body.
- Innate immunity: immediate (0-4hrs)
- infection
- recognition by preformed non specific effectors
- removal of infectious agent (ia) - Early induced response: early (4-96hrs)
- infection
- recruitment of effector cells
- recognition and activation of effector cells
- removal of ia - Adaptive immune response
- infection
- transport of antigen to lymphoid organs
- recognition by naive B & T cells
- clonal expansion of effector cells
- removal of ia
What happens to microorganisms once across the epithelial barrier?
They are recognised & ingested by mononuclear phagocytes or macrophages
Describe each of the following (i) monocyte (ii) neutrophil (iii) eosinophil (iv) basophil.
(i) one of 3 types of phagocytic cel of immune system
- they circulate the bloodstream, becoming macrophages when in tissue.
(ii) (PMN) - most numerous & important cell of innate response
- are v. short lived (2 days)
(iii) (PMN) - parasite defence. Important in getting rid of gut pathogens
(iv) (PMN) - function is similar to that of eosinophils & mast cells. They are the least common PMN.
What are mast cells?
granules.
When releases, they release a number of substances that affect the vascular system
ie. IgE mediated triggering in allergies
Name the two types of lymphocytes and what they produce.
B cells = produce antibodies
T cells = cytotoxic T cells (CD8) OR helper T cells (CD4)
What is the function of dendritic cells?
most important immune cell
they bridge the gap between the innate and adaptive immune response
are specialised in antigen uptake and presentation
What are NK cells? What is their role within the body? How do they stop themselves from destroying healthy cells?
Large granular lymphocytes
Recognise virally infected cells non-specifically
Play and early defence role against viral infection
Have receptors on their cell surface to prvent them from destroying healthy cells.
What is the difference between NK cells and CD8 cells ? (HINT: there’s two)
- NK cells aren’t antigen specific
- NK cells don’t require clonal expansion of T cells in lymph nodes when the virus is detected.
What are the 3 pathways of the complement cascade? Describe each one.
- Classical pathway:
- initiated by activation of the C1 complex
- antibodies binding onto the surface of bacteria
- C1Q acts with the antibody
=> triggering the classical pathway - Lectin pathway
- Alternative pathway:
- cause by spontaneous hydrolysis of serum C3
- this binds to factor B
- factor B is cleaved by factor D into Ba and Bb
- the resulting soluble C3 convertase cleaves C3 -> C3b
- C3b binds to membranes and acts to increase phagocytosis
How is the membrane attack complex (MAC) assembled? What can prevent the final assembly of MAC?
It is comprised of C6, 8, 9 which form a pore
=> the internal contents of bacteria leak out & bacteria dies
CD59 - at the C8 -> C9 stage
What is an atheroma?
degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue, and leading to restriction of the circulation and a risk of thrombosis.
- the fatty material which forms deposits in the arteries.
What are the risk factors associated with atherosclerosis? (HINT: there’s 7)
Age: prime age = 40-60
Sex: males are more predisposed compared to woman PRE menopause
Genetics: diabetes, hypertension
Hyperlipidaemia: increased cholesterol (dietary factors)
Hypertension: more likely
Smoking
Diabetes Mellitus
What is the pathogenesis of atherosclerosis? (HINT: there’s 6)
1. Chronic Endothelial Injury increased: -Endothelial permeability -Leukocyte adhesion -Monocyte adhesion and migration 2. Role of lipids Hyperlipidaemia (LDL cholesterol) – Impairs endothelial function – Accumulates within intima – Causes oxidative modification of LDL: Ingested by macrophages via SCAVANGER receptors = foam cells 3. Role of macrophages Engulf oxidised LDL = foam cells Secret IL1, TNF, MCP1 and growth factors FATTY streak 4. Smooth muscle proliferation Collagen and Extracellular matrix deposition => Fattystreak -> Mature fibro-fatty Atheroma 5. Fibro-lipid plaque formation 6. Injury to plaque: thrombus formation
Describe the morphology of atherosclerosis. Where do they develop? (name a few examples)
Atheromatous plaque > patchy & raised, white to yellow > lipid core, fibrous cap Abdominal aorta coronary arteries popliteal arteries descending thoracic aorta internal carotid artery vessels of circle of willis
What are the complicated lesions that can occur in atherosclerosis?
calcification rupture/ulceration haemorrhage thrombosis aneurysmal dilation
What results in complications within atherosclerosis?
thrombosis
calcification
aneurysmal dilation
ischaemic events
Describe the primary and secondary preventions of atherosclerosis.
Primary (preventing atheroma) - stop smoking - control hypertension - weight loss - lower total LDL (statin) - reduce calorie intake Secondary (one complication has arisen) - prevent complication - anti-platelet drugs in thrombosis - lower blood lipid levels
What is haemostasis?
The arrest of blood loss from damaged blood vessels via:
- vascular constriction
- formation of a platelet plug
- formation of a blood clot (as result of coagulant)
- growth of fibrous tissue into blood clot to close the hole permanently
What is drug therapy used for?
to modify:
- blood clotting
- platelet adhesion & activation
and to affect processes involved in fibrin removal
What are the two ways in which you can develop coagulation defects?
Genetically - haemophilia Acquired - e.g. liver disease, vit K deficiency - treat with either natural or synthetic vitamin K
