blood and immune Flashcards
(L1) what are white blood cells made up of + main functions
neutrophils –> phagocytes (engulf pathogens)
lymphocytes = B & T cells w/ specific receptors
monocytes = sense pathogens
immunology = defence system w/ 2 main functions
1. tolerance - recognising self vs non-self (foreign)
2. seek + destroy foreign (pathogen)
(L1) define:
pathology, pathogen, immune system, immunogenic, antigen, antibody
PATHOLOGY = study of disease + how progress
PATHOGEN = causes disease (eg. bacteria, virus)
IMMUNE SYSTEM = defence to stop pathogen
IMMUNOGENIC = something inducing imm response - humeral (antibody) and/or cell mediated
ANTIGEN = on surface of pathogen, lymphocytes recognise
ANTIBODY = molecular component of imm sys, recognise + bind to antigen
(L1) two main types/parts of immunity are…
INNATE immunity (invariant, always there) and ADAPTIVE immunity (specific to pathogen —> delay)
(L1) innate immunity (2 types)
- EXTERNAL INNATE DEFENCES:
skin, secretions, mucous mem (resp + intestinal tract) - INTERNAL INNATE:
phagocytic cells (migrate first), natural killer cells, defensive proteins, inflammation.
(chemical signalling –>) vasodilation + high permeability of BV –> immune cells enter (–> red, swell etc).
(L1) phagocytes - how they work
damaged cells release histamine –> nearby BV. LEAKY –> fluid assist in clotting + swelling –> phagocytes activated
phagocytes NOT SPECIFIC - recognise almost all bacteria.
enguld bacteria —> (inside) phagosome + lysosome –> phagolysosome —> soluble debris (exits)
(L1) internal adaptive defences overview
SPECIFIC, dependent on lymphocytes (B & T cells)
B cells = develop in bone marrow - make ANTIBODIES
T cells = develop in bone marrow –> mature in thymus. have RECEPTORS. MANY TYPES
REQUIRE ACTIVATION - exposure to specific pathogen.
born with LOTS of DIFF B & T cells - each lymphocyte - diff antigen
MATURATION - more exposure to pathogen = improved affinity to pathogen
specificity RANDOMLY prod by rearrangement of GENES coding for ANTIGEN RECEPTORS (on B&T cells)
(L1) antigen and antigen receptors - characteristics
IMMUNOGENICITY - provoke imm response - stim prod of antibodies or B/T cells
REACTIVITY - react w antibodies/cells it provoked
EPITOPES - ~7 aa (part of antigen) that’s RECOGNISED by B/T / antibody RECEPTORS. several on each antigen
(L1) memory B&T cells - how and what
antigen recognition –> lymphocytes “colonel expansion” - adaptive imm. prod MEMORY B/T CELLS
AFTER exposure –> memory B&Tc. live for decades in lymph nodes. B clone selves + make COPY (memory)
activated on 2nd exposure –. BETTER 2º RESPONSE
(L1) SARS-CoV-2: antibodies and 2 parts
ANTIBODIES: antibodies against prod, but don’t kick in until ~week (ADAPTIVE IMM). so (eg.) RAT tests show VIRUS not antibodies
2 PARTS: used in serology
NUCLEOCASPID = inside - visible when internalised, virus displayed –> antibody response. lots of it.
SPIKE PROTEIN = tip has receptor binding domain (rbd) - interact with host (us) cell –> entry –> infection
(L1) SARS-CoV-2: antibody assays
- Binding antibodies - if antibodies in blood could BIND to spike protein
- Neutralising antibodies - bind to virus –> stop it from entering cells (via receptors)
(L1) SARS-CoV-2: application of antibody assays - 3 applications
- detect historical infections - eg infected a week ago instead of ACTIVE now
- estimate prevalence - serosurvey = testing blood –> prev. of antibodies –> indicates exposure
- understand persistence (how long do antibodies last?) & protection - variants (antibodies sometimes down cross-protect), vaccines help with cross protection after 3 shots
(L2) Blood circulation - veins, arteries, large/small vessels etc.
Venous side (NO pressure) - veins take NO O2 blood –> heart (RIGHT –> LUNGS –> LEFT)
Arterial side (HIGH pressure) - arteries take O2 blood (LEFT) –> body
VEINS: valves so no back flow
LARGE vessels = HIGH vol/LOW flow
SMALL vessels = LOW vol/HIGH flow
BP in capillaries - high enough so no coagulation, low enough to prevent cap leakage; ensure even flow
(L2) 4 main components of blood (+2 other). LITTLE/NO DETAIL
- CELLS - erythrocytes, myeloid (stem), lymphoid
- PROTEINS
- LIPIDS - bound in lipoproteins (LDL = low density lipop., HDL, VDL = very low) measure = indicator of disease
- ELECTROLYTES - isotonicity + buffering. pH TIGHTLY maintained (~7.4)
- vitamins, hormones
- glucose
(L2) 3 of main proteins in blood
- ALBUMIN (50%) - maintains colloidal osmotic pressure (salt balance so no leakage from cap or tissue –> other side) bind + transport hormones/small mol
- FIBRINOGEN (7%) - clotting, activated through coagulation cascade
(L2) centrifugation of blood layers
WITH ANTICOAGULANT from bottom to top: RBC ~40-45% BUFFY COAT - wbc + platelets. PLASMA ~55%
(L2) separation of blood proteins, how it indicated disease + difference between serum and plasma
done by SERUM ELECTROPHORESIS:
electrical field w/cathode & anode –> separation into 5 bands
albumin (closer to anode), globulin ~40% of proteins (alpha 1, a2, beta, gamma = immunoglobulins)
multiple myeloma: leukaemia where B cell prod monoclonal (same) Ig (antibody) –> dark band around antibody region
plasma = viscous liquid w/o cells, + FIBRINOGEN
serum = less viscous liquid w/o cells W/O FIBRINOGEN (w/o clot)
(L2) blood stem cell and what it differentiates into, uses of stem cell
multipotential hemapoietic stem cell (hemocytoblast) in BONE MARROW
CD34+ = surface protein antigen marker on surface of stem cell –> monoclonal antibodies can recognise –> remove stem cell & put back
divide into TWO cells:
1. common myeloid progenitor –> innate system (+RBC)
2. common lymphoid progenitor –> adaptive system
(L2) 3 factors in haematopoiesis
- GM-CSF: (granulocyte macrophage colony stimulating factor) prod BY macrophages, T cells, endothelial cells, fibroblasts. PROD - neutrophils, eosinophils, basophils, monocytes
- EPO: (erythropoietin) prod BY kidney (adult) and liver (perinatal). PROD RBCs
- G-GSF: (w/o M) prod BY many cells. PROD granulocytes + matures neutrophils
(L2) gas transport, pressure differences and effect of cyanide
haemoglobin - comprised of 4 proteins –> each has heme –> heme has Fe2 - binds to O2 at atmospheric pressure
partial pressure of O2 higher in air –> bind
pp of O2 lower in venous sys tissue & pp CO2 higher –> O2 dissociates + CO2 binds to Fe2
CYANIDE - outcompetes O2. binds to Fe2 tightly
(L2) complement and innate immunity. pathway, activation, late stage, why etc.
for PHAGOCYTOSIS
COMPLEMENT = 9 proteins that coat bacteria –> target for phagocytosis
3 pathways to activate complement:
1. CLASSICAL (ANTIBODY) - bind to bacteria surface –> C1 complement bound –> starts cascade
2. lectin
3. alternative
CLEAVAGE of C3 (most abundant) –> active form. small fragments (used to be bound to inactive C) = attract neutrophils
DEPOSITION of convertases (C3 & C5) = OPONISATION. irreversibly covalently bound to surface of bacteria
LATE STAGE - forms lytic pore –> gram - bacteria LYSE. Membrane Attack Complex (MAC)
(L2) coagulation pathway - essential factors, dissolving clot etc.
Ca2+ = essential
prothrombin (inactive) –factor X (enzyme)–> thrombin (active). 2 ways:
1. INTRINSIC - direct contact. eg blood in glass will clot
2. EXTRINSIC - tissue damage
thrombin = ENZYME cleaves fibrinogen –> fibrin (cross links)
(plasminogen –>) PLASMIN = dissolve clot. Tissue plasminogen activators or streptokinase treat thrombosis
parasites & other (eg. mosquitos, leeches) prod anticoagulant - target thrombin step
