blood and immune

Question 1

(L1) what are white blood cells made up of + main functions

Answer 1

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)

Question 2

(L1) define:

pathology, pathogen, immune system, immunogenic, antigen, antibody

Answer 2

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

Question 3

(L1) two main types/parts of immunity are…

Answer 3

INNATE immunity (invariant, always there) and ADAPTIVE immunity (specific to pathogen —> delay)

Question 4

(L1) innate immunity (2 types)

Answer 4

1. EXTERNAL INNATE DEFENCES:
   skin, secretions, mucous mem (resp + intestinal tract)
2. 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).

Question 5

(L1) phagocytes - how they work

Answer 5

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)

Question 6

(L1) internal adaptive defences overview

Answer 6

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)

Question 7

(L1) antigen and antigen receptors - characteristics

Answer 7

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

Question 8

(L1) memory B&T cells - how and what

Answer 8

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

Question 9

(L1) SARS-CoV-2: antibodies and 2 parts

Answer 9

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

Question 10

(L1) SARS-CoV-2: antibody assays

Answer 10

1. Binding antibodies - if antibodies in blood could BIND to spike protein
2. Neutralising antibodies - bind to virus –> stop it from entering cells (via receptors)

Question 11

(L1) SARS-CoV-2: application of antibody assays - 3 applications

Answer 11

1. detect historical infections - eg infected a week ago instead of ACTIVE now
2. estimate prevalence - serosurvey = testing blood –> prev. of antibodies –> indicates exposure
3. understand persistence (how long do antibodies last?) & protection - variants (antibodies sometimes down cross-protect), vaccines help with cross protection after 3 shots

Question 12

(L2) Blood circulation - veins, arteries, large/small vessels etc.

Answer 12

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

Question 13

(L2) 4 main components of blood (+2 other). LITTLE/NO DETAIL

Answer 13

1. CELLS - erythrocytes, myeloid (stem), lymphoid
2. PROTEINS
3. LIPIDS - bound in lipoproteins (LDL = low density lipop., HDL, VDL = very low) measure = indicator of disease
4. ELECTROLYTES - isotonicity + buffering. pH TIGHTLY maintained (~7.4)
5. vitamins, hormones
6. glucose

Question 14

(L2) 3 of main proteins in blood

Answer 14

1. ALBUMIN (50%) - maintains colloidal osmotic pressure (salt balance so no leakage from cap or tissue –> other side) bind + transport hormones/small mol
2. FIBRINOGEN (7%) - clotting, activated through coagulation cascade

Question 15

(L2) centrifugation of blood layers

Answer 15

WITH ANTICOAGULANT
from bottom to top:
RBC ~40-45%
BUFFY COAT - wbc + platelets.
PLASMA ~55%

Question 16

(L2) separation of blood proteins, how it indicated disease + difference between serum and plasma

Answer 16

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)

Question 17

(L2) blood stem cell and what it differentiates into, uses of stem cell

Answer 17

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

Question 18

(L2) 3 factors in haematopoiesis

Answer 18

1. GM-CSF: (granulocyte macrophage colony stimulating factor) prod BY macrophages, T cells, endothelial cells, fibroblasts. PROD - neutrophils, eosinophils, basophils, monocytes
2. EPO: (erythropoietin) prod BY kidney (adult) and liver (perinatal). PROD RBCs
3. G-GSF: (w/o M) prod BY many cells. PROD granulocytes + matures neutrophils

Question 19

(L2) gas transport, pressure differences and effect of cyanide

Answer 19

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

Question 20

(L2) complement and innate immunity. pathway, activation, late stage, why etc.

Answer 20

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)

Question 21

(L2) coagulation pathway - essential factors, dissolving clot etc.

Answer 21

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