Blood

How is plasma different to intersititial fluid?

Contains proteins, plus high heat holding capacity aids thermoregulation

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Which plasma proteins are produced in the liver?

Albumins (abundant, generate oncotic pressure), globulins (clotting factors, enzymes, antibodies and immunglobulins), fibrinogen

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Where is transferrin (for Fe transport) formed?

Lymphoid tissue

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Where are erythrocytes removed?

After 120 days by liver and spleen

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What holds the biconcave shape of erythrocytes?

Spectrin and actin in the cell cortex

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Why do RBC's have no mitochondria?

To increase space for Hb - gain energy from glycolysis

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Wat does a low PCV indicate?

Anaemia, overproduction of WBC's or blood loss

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What does a high PCV indicate?

Dehydration, diarrhoea, lung or heart disease (reduces PO2 so increased RBC production), polycythaemia vera (icreased RBC production), high altitudes or doping

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How is serum generated?

When the anticoagulants are removed from blood/when it is left to clot - though doesn't contain cells/clotting factors has major proteins and smaller molecules (used in diagnostics)

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What are the causes of oedema?

Lymph node obstruction through tumours or parasites, or lymph node removal in cancer treatment; also through increased hydrostatic pressure in heart disease, increased oncotic pressure in malnutrition/liver disease or ICF proteins in inflammation.

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What is haematopoiesis?

Blood cell formation in bone marrow; stimulated by cytokines (EPO from kidney, TPO from liver) causing pluoripotent haematopoietic stem cell (PHSC) differentiation

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What do neutrophilic granules contain?

Lysosomal enzymes for phagocytosis

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Decsribe the nuclei of the different white blood cells

Neutrophils = multi-lobular, basophils and eosinophils = double-lobed, monocytes = indented

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What substances produced by leukocytes stimulate blood cell growth?

Colony-stimulating proein (also from endothelium and bone marrow fibroblasts, mobilises PHSC's) and interleukins (mobilise PHSC's to produce more of same leukocytes for rapid infection control). Stem cell factors from fibroblasts also mobilise PHSCs.

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Describe the process of erythropoiesis

EPO from kidney fibroblasts when hypoxia simulates HIF-1 transcription factor --> bone marow proerythroblasts --> erythroblasts, nucleus lost + enter blood --> reticulocytes, lose miochondria + ribosomes --> erythrocytes. Takes 24hrs.

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How is megakaryocyte production inhibited?

Platelets bind to TPO so it is destroyed, meaning megakaryocytes can be formed from megokaryoblasts (and fragment to form platlets)

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Describe granulopoeisis (production of granulocytic WBC's down myeloid line)

Myoblast forms from myeloid progenitor in bone marrow, granules begin to appear to determine cell type

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What do eosinophilic granules contain? What is the function of eosinophils?

Granules have major basic protein so stain red with acidic eosin. Fight viruses/parasites, play role in allergic reactions.

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What do basophilic granules contain? What is the function of basophils?

Granules have hisamine, heparin and peroxidases so stain blue with eosin. As mast cells in tissues instigate allergic reactions (see later).

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Describe monopoiesis (formation of monocytes down the myeloid line)

Monoblast progenitors from PHSC's in bone marrow --> monoblasts --> promonocytes --> mature monocytes --> macrophages in tissues (perform phagocytosis, present antigens to lymphocytes)

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Decribe leukopoiesis (formation of leukocytes down lymphoid line)

PHSC's form leukocyte stem cells (common lymphoid precursor cells) --> in blood develop into pro-B or pro-T lymphocytes (identified by their large nuclei)

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What are CD (cluster of differentiation) proteins?

Specific to cell membrane of certain cell types so can be used to differentiate between them

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What is immunophenotyping?

Uses antibodies complientary to CD proteins to identify blood cells (and therefore blood type)

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Why may people require blood transplants?

Destruction of uncommitted stem cells in chemotherapy, bone marrow failure (severe aplastic anaemia), blood disorders (sickle-cell anaemia), Non-Hodgkins Lymphoma (spreads through lymphatics) or leukaemia

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What is acute onset leukaemia?

Bone marrow rapidly releases many immature WBC's

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What is chronic onset leukaemia?

Relatively mature WBC's are released over a long time

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What are the symptoms of (lymphoblastic or myeloid) leukaemia?

Purpura (purple spots caused by bleeding under skin), gingival bleeding/swelling, ulceration, infections (candidiasis and herpes), anaemia and thrombocytopenia (reduced platelets)

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What is ferratin?

Excess store of Fe bound to transferrin; can be toxic in large amounts (when not transported to bone marrow to release iron for erythropoiesis)

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What is the fate of bilirubin (waste product of RBC's)?

Formed in the spleen (with some haem being recycled); then some released to kidney for excretion in urine, rest goes to liver to form bile. Ineffective removal in jaundice (usually when foetal Hb converted to adult Hb early).

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What is the Bohr effect?

Exercise forms lactic acid, decreasing blood pH so Hb affinity for O2 reduced (causing release to tissues)

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What is HBA1C/glucohaemoglobin?

Where Hb has irreversibly bound to glucose; can measure glucose fluctuations over 8-12 weeks

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What are heamoglobinapathies?

Diseases caused by mutation in globin gene; example is sickle cell anemia where glu-->val in B globin, forming HbS (with 20 day lifespan, forms intracellular precipitates so cells cresent shape)

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What are thalassaemias? Give examples?

Normal globin chains in wrong amounts; means large spleen, anaemia, poor growth. A-thalassaemia = less A-globulin (more B-globulin = unstable tetramers). B-thalassaemia = less B-globulin (more A-globin = no tetramers, RBC membrane damage, aggregates)

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What is anaemia?

Clinical sign, low Hb for age/ethnicity/sex (less than 13.5g/dl in men, 11.5g/dl in women). Causes lethargy, headaches, cardiorespiratory consequences, pallor, koilonychas (spoon nails), glossitis, ulceraion, angular stomatitis.

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What is MCV (mean corpuscular volume)? How is it calculated?

Mean volume of each RBC (in fl, femto = x10-15). Usually 76-96fl. Calculated by RBC volume (L)/No RBC's per L.

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What is MCH (mean corpuscular Hb)? How is it calculated?

Average Hb content of RBC's (units pg, picto = x10-12). Usually 27-32pg. Calculated by Hb in g per L/No RBC's per L.

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What is MCHC (mean corpuscular Hb conc)? How is it calculated?

Conc of Hb in the blood (units g/100ml, usually 30-35). Calculated by Hb in g per 100ml/PCV as decimal.

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Describe a red blood cell count

Gives number RBC's per L. RBC's counted under microscope using haematocyometer; given by No cells/square x square V x blood dilution factor (200). Usually 4.5-6.5(x10-12) in men, 3.8-5.8(x10-12) in women.

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How is Hb conc gained?

Blood and Drabkin's solution mixed in cuvette and left for 10min. Colour analysed by spectrophotometer, conc gained by plotting on graph/comparing with British standard solution. In males usually 130-180g/l, in females usually 115-165g/l.

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What is microcytic anaemia?

Small RBC's which are hypochromic through low MCV and MCH. Cause Fe deficiency as lacking/high phyate/low Vit C diet or malabsorption. Chronic haemorrhage (via NSAID's, stomach ulcers/cancer) seems similar. Serum ferratin low, platelets raised.

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What are the causes of noromcytic anaemia (MCV and MCH normal)?

>2 pints rapid blood loss, haemolysis (RBC destruction) or bone marrow disease. eticulocytes hig as erythropoiesis udergoing to replace lack.

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What causes macrocytic/megaloblastic anaemia (high MCV)?

B12/folate deficiency. Cells expess asynchrony (nucleus immature so cell doesn't divide but still cytoplasm accumulation); creates megaloblastic cells which aren't biconcave and have reduced lifespans. Cell frgaments likely and RBC count low.

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What is the difference between haem and non-haem iron?

Haem = Fe2+ from myoglobin/Hb in meats (which contain absorption promoters like Vit C, citric acid and alcohol). Non haem = Fe3+ from eggs/veg (contain inhibitors of absorption like phyates, phosphates and tannins)

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What iron supplements are given?

Ferous sulphate (600mg/day for 3 months) or to reduce tooth staining/erosion sodium iorn edetate

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How is DNA synthesis reduced in Vit B12 deficiency?

Less than 20ug/day over 2 years --> B12 deficient --> methionie synthase not activated (via homocystiene-->methionine) --> no 5-methyfolate to tetrahydrofolate. Traps folate so can't be used in DNA synthesis; appears as secondary folate deficiency.

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How is DNA synthesis reduced in folate deficiency?

No folate --> dihydrofolate --> tetrahydrofolate --> 5,10-methylfolate. Means no 5,10-methylfolate back to dihydrofolate, so no simultaneous dUMP-->dTMP (for DNA synthesis). MCV high/WBC nucleus fragmented.

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Wha is pernicous anaemia?

Increased anibodies specific to parietal cells so they regenrate, preventing intrinsic factor production so no B12 absorbed. Alternatively, increase may be in antibodies complementary to IF. Red tongue/ulcers occur. Gastric parietal antibody high.

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How is pernicious anaemia diagnosed?

To ensure not through gastritis/>40 years, perform Shilling test. Small radioactive B12 dose, after 2hrs big normal B12 dose. 24hr urine collection, if radioactive B12 15%.

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What is pancytopenia?

Malfunction of bone marrow so all blood cells reduced; caused by cancer, autoimmue malfuctions, viruses and drugs. Causes aplastic anaemia (RBC's nomocytic and normochromic).

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What is haemocytic anaemia?

Caused by excess RBC destruction; due to abnormal Hb/RBC membranes, G-6-dehydrogenase deficiency causing oxidative stress, autoimmue fuctions, drugs or infection. Hb conc low, reticulocytes raised to replace, polychromasia and irregular RBC shapes.

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What are spherocytes and schistocytes?

Spherocytes = spectin mutation creates round RBC's, schistocytes = show fragmentation. May appear in haemolytic anaemia (as cause for RBC destruction).

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What is haemostasis?

Stoppage of blood flow out of a damaged vessel whilst still allowing blood to flow within it

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Why is vasoconstriction the first step in haemostasis?

Increasing pressure so sufficient seal can be made (the repair patch isn't too weak). Stimulated by hormonal signals from paracrines to cause arterial walls to constrict (vital as O2 supply more important than venous collapse (and no smooth muscle))

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What are the features of platelets?

Frequent, high turnover, 1000 from one megakaryocyte, no nucleus, 20% size RBC's, live 8-12 days.

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What granules do platelets contain?

Have alpha granules (with fibrinogen, VWF, V and other factors (attract WCB's/smooth muscle/fibroblasts)) and dense granules (with ADP (activates platelets), ATP, clacium and serotonin (vasoconstrictor and aggregating agent)).

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How does the platelet plug form?

Collagen exposure in ECM and VWF from damaged endothelium/megakaryocytes --> platelets adhere to collagen via integrin and each other --> platelets activated (become spiky) so release granules --> platlet activating factor activates more

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What releases platelet activating factor?

Neutrophils, monocytes (macrophages in tissues), the platelts themselves - means another activation element so plug formed quickly

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What occurs in the intrinsic coagulation pathway?

Uses substrates already present in blood. Collagen exposure activates XII, aXII activates XI, aXI activates IX, aXI combines with aVIII (activated by VWF) and Vit K --> common pathway

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What occurs in the extrinsic coagulation pathway?

Uses substrates made on demand. Damaged endothelium releases thromboplastin (III), which activates VII. aVII and III and Vit K ---> common pathway

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What occurs in the common coagulation pathway?

At start products of intrinsic and extrinsic pathways (plus Ca2+ and phospholipids) activate X. aX converts prothrombin to thrombin; this converts fibrinogen to fibrin and activates XIII (which cross-links fibrin).

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Where does positive feedback occur in the coagulation pathway (to accelerate it)?

Thrombin activates XI (in intrinsic pathway) and aX causes activation of VII (in extrinsic pathway)

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How does anticoagulation occur?

Healthy endothelium releases NO and prostacyclin to prevent platelet adherence and inhibit the coagulation pathway. Fibrin production prevented when anticoagulants released into endothelial cells.

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Give examples of anticoagulants

Heparin, anti-thrombin and thrombomodulin (block thrombin, IX, X, XI and XII) and protein C (blocks V and VIII)

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What is fibrinolysis?

Stops clots blocking flow; fibrin (and fibrinogen) fragments broken down by plasmin (when plasminogen activated by thrombin and tissue plasminogen activator to from plasmin). Fibrin degradation products are released, also act as anticoagulants.

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What causes thromboembolic episodes (inapropriate clots)?

Scarring (atherosclerosis), prosthetic heart valves, varicose veins (slow blood) and altered blood factors (DIC). Pieces of clots form emboli which block vessels.

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What is dissembled vascular coagulopathy (DIC)?

Large factor III release during trauma; produces many micro-clots which use up all factors/fibrin/platelets so reduced coagulation prevents sealing of serious damage

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Give examples of anticoagulation drugs

Treatments for myocardial infarction (tissue plasminogen activator and anti-platelet drugs, prevent platelets binding integrin), aspirin (prevents platelet plug) and warfarin (blocks Vit K)

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What is thrombocytopenia?

A thrombopathy (platelet disease) where platelet count is low due to bone marrow supression (in leukaemia/chemotherapy)

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What is thrombocythaemia?

Thrombopathy where platelets overproduced, though these are prone to poor clotting

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What is haemophilia?

X-linked recessive disease causing reduced fibrin production as a clotting factor is defective/lacking (VIII in type A (more common), IX in type B). This means sufferes produce a platelt plug but no clotting so useless; causes spontaneous bleeding.

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What is Von-Willebrand disease?

Lack of VWF so platelet adhesion reduced and intrinsic coagulation pathway inhibited (VIII isn't activated). Common, causes nosebleeds, gingival/post-surgery bleeding and anaemia.

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What is bleeding time?

Time taken to form platelet plugs. 40mmHg applied using blood cuff, vessels severed, time for bleeding to stop measured (usually 3-8mins). High = VWF deficiency/thrombocytopenia.

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What is prothrombin time (PT)?

Measures common and extrinsic pathways. Fibrin formation of plasma measured at 37o in high III concentration; time for recalcification by adding CaCl2 (initiates clotting) measured. Normally 10-14 sec.

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What is thrombin time?

Mesures common pathway. Thrombin added to plasma at 37o, time for coagulation measured and compared to control. Usually 10-12 sec.

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What is activated partial thromboplastin time (APTT)?

Measures intrinsic and common pathways. Time for fibrin formation measured upon recalcification of plasma in the presence of kaolin (optimises activation reactions); compared to a control. Normally 38-45 sec.

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What determines your ABO blood group?

Genotype determines which glucotransferase formed, therefore how glycoprotein H modified. Inactive glucotransferase = GlyH unmodified = O. A glucotransferase = GlyH with antigen A = A. B glucotransferrase = GlyH with antigen B = B.

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What is self tolerance?

Early in life only antibodies to A/B antigens NOT possessed by RBC's are produced. This means no immune response is produced to the antigens posessed (blood type) in transfusions; others (first experienced in gut flora/food) cause agglutination.

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What occurs in agglutination?

Antibodies of recipient bind to donor RBC's causing them to aggregate so their function is prevented (also causes vessels to block). To prevent, donor blood must have no antigens recipent has antibodies to (recipient serum/donor RBCs tested first)

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Which ABO blood group is the universal donor?

Group O as they have no antigens on their RBC's which can be recognised by recipient antibodies. However, can only recieve from group O as has both A and B antibodies.

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Which ABO blood group system is the universal recipient?

AB as have neither A or B antibodies so can recieve any RBC's; however can only dontate to AB as any other group has at least one antibody against their A and B antigens.

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Describe the Rhesus blood group system

Individuals Rh+ve (heterozygous or homozygous dominant) have D antigen on RBC's. Rh-ve individuals (homozygous recessive) have no D antigens on their RBC's. Must be tested for before transfusion as Rh-ve would make antibodies against D antigens.

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What is a haemolytic transfusion reaction?

Occurs when Rh-ve given RH+ve RBC's. Causes erythrocyte agglutination, intravascular coagulation and RBC lysis (through compliment activation) causing kidney failure.

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What is haemolytic disease of the newborn?

Upon repeated incidence of Rh-ve mother with Rh+ve baby (so secondary response against D antigen of infant); anaemia in child through RBC lysis. Prevented by early anti-Rh antibody injection into mother (surrounds D antigens so unrecognised).

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Why are blood groups no longer used in paternity testing?

Can only exclude (not identify) fathers; now use microsatellite DNA fingerprinting

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What are major histocompatibility proteins?

These instigate the recognition of foreign blood lymphocytes. They are very polymorphic (similar only in twins/siblings); must be matched before organ transplantation to prevent graft-vs-host disease (T-cells attacking donor tissue).

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What is innate immunity?

Present constantly in everyone, provides frontline defence against infection. Not specific, doesn't change after exposure and no immunological memory.

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What does the innate immune response involve?

Physical/chemical barriers to infection (epithelia with tight junctins/cilia/keratin, mucous, pH extremes (gastric acid/skin), lysozyme enzymes in tears/saliva and temp increases (activate immunity/inhibit bacteria). Also phagocytosis and compliment.

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How do macrophages stimulate innate/adaptive responses?

Release of cytokines

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What is opsonisation?

Bacteria with capsules coated by antibodies so can be recognised and phagocytosed

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What is compliment activation?

Element of innate immuunity; series of blood proteins activated which can opsonise bacteria, aid inflammation and lyse bacteria (so must be highly regulated to prevent host cell damage).

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What is primary phagocytosis?

Large neutrophil reserves in bone marrow released to blood; at infection site endothelial cells migrate to allow passage of neutrophils and tissue fluid (causing swelling). Neutrophils phagocytose bacteria, die and are degraded by macrophages.

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What occurs in inflammation?

Excessive primary phagocytosis resulting in fever, redness, swelling, pain and function loss. May be due to chronic infection, autoimmune diseases (diabetes), hypersensitivity, metabolic disorders (obesity/COPD) and immunodeficiency.

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What is adaptive immunity?

Specific response, reacts to unique foreign antigens. Takes 4-5 days for primary response (humoral and cellular immunity), most effective in secondary response (memory B cells recognise, rapidly produce plasma cells so antibodies higher/longer).

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What is humoral immunity?

B lymphocytes differentiate into plasma cells which secrete antibodies complimentary to the antigen

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What is cellular immunity?

T cell binds via surface receptors to antigens presented by MHC proteins on antigen presenting cells (macrophages/dendritic cells), activating it. Cyotoxic T-cells induce apoptosis of virally infected cells, T helper cells secrete cytokines.

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What are the roles of cytokines released from T helper cells?

Th1 cells release cytokines aiding phagocytosis by macrophages, Th2 cells release cytokines which activate more B cells

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What is the role of mast cells?

Cause tissue changes in response to antibodies, provide immunity to parasites and cause hypersensitivity

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What do antibodies cause?

Opsonisation, agglutination of phagocytes, neutralisation of toxins and compliment activation

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Give examples of monoclonal antibodies

Herceptin (acts on HER2 receptors - which increase growth - to treat breast cancer) and infliximab (blocks action of TNF proteins which cause swelling/inflammation in rheumatoid arthritis)

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What is necrotising ulcerative gingivitis?

Caused by poor immune response; microbial, associated with stress, smoking, HIV and nutritional deficiencies

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What does Hepatitis B cause?

Compromised immune response resulting in liver inflammation/failure

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What occurs in HIV?

Virus kills helper T cells

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Whay occurs in Ebola?

Dendritic cells infected

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Blood

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