BLOOD Flashcards
1
Q
PLASMA
A
- plasma is water (90%-92%)
> Plasma protein (7% of plasma)
> electrolytes
> nutrients (digesting foods)
> waste products
> hormones
> gases
2
Q
PLASMA PROTEIN
A
- protein is synthesised in the liver
- exceptions of immunoglobins (antibodies)
- produced by B-cells of the immune system
- too big to escape through the capillary wall into the tissue & plasma proteins are retained through the bloodstream
- maintaining through osmotic pressure of blood
- plasma levels fall: reduce production/loss from blood vessels, osmotic pressure is reduced, fluid shifts into the tissue (oedema)
- plasma proteins are
> albumins
> globulins
> Fibrinogen (the blood clotting protein)
3
Q
ALBUMINS
A
- plasma protein (60%)
- maintain normal plasma osmotic pressure
- acts as a carrier molecule for fatty-free acids
4
Q
GLOBULINS
A
> antibodies (immunibologins) complex protein produced by lymphocytes
- play an essential role in immunity
- bind to & neutralise foreign materials (antigens, e.g. micro-organisms)
Transport globulins: bind to transport hormone and mineral salts into the bloodstream
5
Q
FIBRINOGEN & OTHER CLOTTING PROTEINS
A
- fibroinogen is the most abrundant
- A blood sample not treated with an anticoagulant begins to clot when exposed to air.
- soft clot that sticks to the bottom of the container
- clear-straw coloured = sternum
- sternum and plasma are similar, except the sternum has little or no clotting protein left.
6
Q
ELECTROLYTES
A
- +ve charged ions in blood sodium
- the main anion -ve charged ions = chloride Cl-
- electrolytes have a range of functions muscle contraction
- blood pH is maintained between 7.35 and 7.45 (slightly alkaline) = ongoing buffer system
7
Q
NUTRIENTS
A
- substance essential for growth
- metabolism: including glucose, amino acid & vitamins transported in the blood stream
8
Q
WASTE PRODUCTS
A
> urea (waste product)
creatinine (waste product)
- formed in the liver
- carried through the blood to the kidneys
- carbon dioxide from tissue metabolism transported to lung through kidney
9
Q
HORMONES
A
- chemical messengers synthesised by an endocrine gland
- secreted directly into the bloodstream, transports them to their target tissue and organs
10
Q
GASES
A
- less than 2% is dissolved in plasma
- O2 bound to haemoglobin in red blood cells
- 98% of O2 in blood is carried as oxyhaemoglobin
- haemoglobin binds to carbon dioxide most carbon dioxide is converted to bicarbonate ions in red blood cells
- then transported into the plasma
11
Q
CELLULAR CONTENT OF BLOOD
A
> erythrocytes (red blood cells)
Leukocytes (white blood cells, e.g. neutrophils, lymphocytes, basophils)
platelets (thrombocytes)
- produce in red blood marrows
- lymphocytes are produced in lymphoid tissue
- each type of blood follows a separate line of development process of blood formation = haemopoiesis
CHILDREN: red bone marrow fills the space between the bone and produces enough blood cells to meet the needs of growing children
- 20 years replaced with fatty yellow marrow with no haemopoietic fucntion
12
Q
ERTHYOCYTES (RED BLOOD CELLS)
A
- 99% of blood cells = red blood cells
- red blood cells = thin, flattened biconcave discs = no nucleus
main role: - transport: respiratory gases, O2, carry carbon dioxide
- biconcavity increases surface area for gas exchange
- cells are flexible to fold and squeeze through narrow capillaries = no intercellular organelles
- protein = responsible for gas transport
- flattered shape, allowing staking to happen
- streamlining blood flow and reducing turbulance
13
Q
LIFESPAN & FUNCTION OF ERYTHOCYTES
A
- have no nucleus
- erythrocytes cant divide into the bloodstream
- balancing production in red bone marrow broken down in the liver
- erythrocytes development from stem cells = 7 days = erythropoiesis
- immature cells are released into the bloodstream as RETHICYTES red blood cell synthesis
- vitamin B (cobalmin) bound to intrinsic factors
- folic acid required for red blood cell synthesis
- absorbed into the small intestine
- vitamins dairy products, meat and green vegtable
14
Q
HAEMOGLOBIN
A
contains: globular protein (globin)
- pigmenting ion-containing complex called haem
- haemoglobin molecule contains four globin chains and four haem units
- iron can combine with an O2 molecule single haemoglobin = carry up to four molecules of O2
- iron is carried into the bloodstream bound to transport protein stored in the liver
15
Q
OXYGEN TRANSPORT
A
- o2 binding sites
- haemoglobin binds to oxygen = oxyhaemoglobin
haemoglobin + oxygen - oxyhaemoglobin
- blood = bright red because of the high level of oxyhaemoglobin
- oxyhaemoglobin releases its oxygen readily under certain conditions: low, pH, low oxygen and raised temperature
16
Q
LOW pH
A
- Metabolically active tissue
- release acid waste product
- oxygenhaemoglobin break down giving up + O2 for tissue use
17
Q
LOW O2 LEVELS
A
- levels = low
- oxygenhaemgoboin levels = lower than the blood
- HYPOXIA = O2 levels in the blood or tissues
- HYPOXIA conditions: oxygenhaemoglobin dissociates = increasing O2 supply in the cell
- O2 levels are high in the lungs, oxygenhaemoglobin
18
Q
HIGHER TEMPERATURE
A
- Active tissue receives a higher O2 supply than less active tissue
- LUNGS alveoli are exposed to air, and the temperature is lower
19
Q
CONTROL OF ERYTHROPISES
A
- red cells = consististnat
- Bone marrow produces erythrocytes
- hormones that regulate red blood cells = erythropoietin = produced by kidneys
- erythropoiesis = hypoxia
- Hypoxia develops in situations = anaemia, reduced blood volume, poor blood flow = stimulation erythropoietin increases erythrocyte production & restoring O2 supplies in tissue
- erythropoietin = increase production of proerythroblast = release of reticulcocytes into the blood
- O2 carrying capacity of blood & reverse tissue = hyproxia
- With no erythropoietin, erythrocyte production declines in the presence of hypoxia
20
Q
DESTRUCTION OF ERTHROCYTES
A
- The cell membrane becomes more fragile & more susceptible to rupture
- erythrocyte breakdown, triggering blood clotting and an inflammatory response
- ageing erythrocytes extracted from circulation by macrophages
- Iron released by haemoglobin breakdown = returned to the bone marrow for haemoglobin synthesis
- haemoglobin = breakdown to green pigment = biliverdin
- yellow pigment = bilirubin, before binding to the liver globulin = transported to liver
- Liver bilirubin is converted from fat-soluble to water-soluble from to be extracted to bile
21
Q
BLOOD GROUPS
A
- The erythrocyte membrane carries various proteins (antigens) = immune response. transported to the bloodstream
- Antigens inherited from parents determine the individual’s blood group
-transfusion:
> same blood type = will not be seen as foreign and will not be rejected
> Different blood group = the immune system generates antibodies and destroys the transfused cells - Red cell surface antigens are most important in ABO and the Rhesus system
22
Q
ABO SYSTEM
A
- 55% of people in the UK = blood group A, group B or group AB
- 45% don’t have A/B, they will have -A or -B
- Group A cannot produce antibodies for -A
- -B antibodies, B antigens are non-self and foreign, group B only makes -A
- Blood group AB makes neither antibodies
- Blood group O makes both anti-A and anti-B antibodies
Group O is known as a universal donor - Donor erythrocytes may be foreign to recipients = transfusion reaction
- Cross-matching before transfusion is required, ensuring no blood reaction between the donor’s & recipients blood
23
Q
THE ABO SYSTEM
A
24
Q
RHESUS SYSTEM
A
- erythrocytes membrane antigen = important to rhesus factor
- 85% of people have this antigen rhesus +, and don’t make anti-rhesus antibodies
- 15% have no rhesus antigen = rhesus-negative
25
LEUKOCYTES
- defence and immunity
- Detect foreign or abnormal materials and destroy them
- Leukocytes are the largest blood cells
- make up 1% of the blood
- They contain nuclei, and some have granules in the cytoplasm
> granulocytes
3 types:
- Eosinophils take up the red dye eosin
- Basophils take up alkaline
- neutrophils squeeze through capillary walls
(polymorphonuclear leukocytes (neutrophils) (basophils)
> agranulocytes - monocytes & lymphocytes = increasing leukocytes in bloodstream
26
NEUOPHILIS
- Fast & active scavenging protects the body from bacteria
- Remove dead cells from damaged tissue
- attract infections by chemicals = chemotaxis - released by damaged cells
- squeeze through the capillary wall
- nuclei = complex 6 lobes
- Granules = lysosome enzyme to digest
- live up to 5 days in the bloodstream
-
27
ESOINOPHLS
- role: elimiation of paracities
- Toxic chemicals stored in granules are released when eosinophils bind to an invading organism
- eosinophils = occur in allergic inflammation, i.e. asthmatic airways and skin allergies
28
BASOPHILS
- allergic reactions to heparin (anticoagulant), histamine (inflammatory agent)
- binds to antibody-type receptors on the basophil membrane, triggers release of the basophil's inflammatory mediators
29
MONOCYTES
- the largest of white blood cells
- released from red bone marrow - migrate to tissue and develop into macrophages
- monocytes & macrophages = interleukin1:
> acts on hypothalamus = fever (pyrexia) = microbial infections
> interleukin1 = pryrogen
> stimulates the production of globins in the liver,
> enhances the production of activated T- T-cells (immunity)
30
THE MONOUCLEAR PHAGOCYTES SYSTEM
- reticuloendothelial system & consists of monocytes & monocytes
- Macrophages have a diverse range of protective functions. Actively phagocytic
- The synthesis and release of an array of biologically active chemicals = interleukin-1
- role: linking non-specific and specific (immune) systems of body defence & produce and repair
31
LYMPHACYTES
- Some circulate in the blood, but most are found in tissue (lymphatic tissue)
- Lymphocytes develop from pluripotent stem cells in red bone marrow
- production of two distinct types of lymphocytes, T-lymphocytes and B-lymphocytes
32
PLATELETS (THROMBOCYTES)
- disc-shaped cell fragments
- budded off the cytoplasm of megakaryocytes in bone marrow
- containing all substances essential for blood clotting = homeostasis
- actin fibres = platelets within the developing clot to retract
- The mechanism regulates the platelet numbers is not understood = hormone thrombopoiesis = liver stimulating platelet production
33
HAEMOSTASIS
- blood vessels = damaged = blood lose stopps and healling happenes
34
VASOCONSTRICTION
- Platelets come into contact with damaged blood vessel walls
- The walls become sticky
- Then release serotonin & thromboxanes
- constructing the blood vessel and stopping blood flow
35
BLOOD CLOTTING FACTORS
36
PLATELET PLUG FORMATION
- Sticky platelets clump together
- releasing substance: adenosine, diphosphate = reaction in the platelet site
- passing platelets stick to damaged vessels = release of chemicals
POSITIVE FEEDBACK SYSTEM
- vascular damage and quickly forming temporary seal
37
COAGULATION (BLOOD CLOTTING)
- clotting factors = enzymes = produced in the liver & circulates as inactive forms in the bloodstream
- resulting in the formation of prothrombin activator
- Prothrombin activates the enzyme, which converts into inactive fibrinogen
- clot traps cells and other plasma proteins, including plasminogen
EXTRINSIC PATHWAY:
> Activated rapidly following damage
> damaged tissue released a complex of chemicals = thromboplastin
INSTINCT PATHWAY:
> pathway is slower
> triggered when blood comes into contact with a damaged blood vessel lining
- clot shrinks actin fibres, the platelets contract, squeezing out the serum
- clot retention pulls the edge of the damaged vessels together, reducing blood loss and closing off the hole in the vessel wall
38
THROMBOLYSIS
- breakdown of fibroin
- plasma protein = plasminogen = inactive precursors of the active enzyme plasmin, which clots as it forms
- converted to plasmin by activators released from the damaged endothelial cells
- Plasmin breaks down fibrin = removing clots to allow tissue repair
39
CONTROL OF COAGULATION
- clotting relies heavily on self-perpetuating processes
- Positive feedback mechanisms promote continuation
- Control and braking mechanisms are essential to clotting to the affected area
factors:
> endothelial lining (healthy, undamaged blood vessels)
> activated clotting factors = rapid deactivated by anticoagulants = heparin
> activated clotting factors cleared from the blood by the liver
40
ANEMIAS
- The blood doesn't carry enough O2 to meet the body's needs
- due to low haemoglobin levels, but caused by the production of faulty haemoglobin
Factors of anaemias:
> production of insufficient or defective erythrocytes - red blood cells being released is too low or red blood cells are defective, the O2 carrying capacity of the blood is reduced = iron deficiency, vitamin B & bone marrow failure
> blood loss/erythrocyte breakdown (haemolysis), anaemia develops if erythrocytes are lost from circulation
- Anaemia may exist with a normal red blood cell count and no abnormalities of erythrocyte structure (normochromic normocytic anaemia)
signs and symptoms: insufficient O2, fatigue & breathlessness on excursion
> tachycardia = heart rate increased to improve blood supply
> palpitation or angina pectoris - increased of efforts of overworked heart muscles
41
CHARACTERISTICS OF RED BLOOD CELLS
NORMOCHROMIC: cell colour normal
NORMOCYTIC: cells are normal-sized
MICROCYTIC: cells are smaller than normal
MACROCYTIC: cells bigger than normal
HYPOCHROMIC: cells are paler than normal
HAEMOLYTIC: rate of cell destruction raised
MEGALOBLASTIC: cells are large and immature
42
IRON DEFICIENCY ANAEMIA
- Red blood cell count is often normal, small, and pale
- contain less haemoglobin than normal
- iron deficiency anemia can = from deficient intake high iron requirements or poor absorption from the alimentary tract
43
DEFICIENCY INTAKE
- relative inefficiency of iron absorption, deficiency = common
- develops slowly
- risk of deficiency if diet is restricted, e.g. poorly planned vegan/vegetarian diets
44
HIGH REQURIMENTS
- increased to support both fetal and maternal growth of the cardiovascular system
- peptic ulcers, heavy menstrual bleeding (menorrhagia)
- Iron intake may be restricted if they are fussy eaters or raised on a poor-quality diet
45
MALABSORPTION
- dependent on the acidic environment in the stomach, gastric pH
- Parietal (acid-releasing) cells in the stomach lining are destroyed
- loss of surface are for absorption in the intestine
46
VITAMINS/FOLIC ACID DEFICIENCY ANAMIAS
- Abnormally large erythrocytes (megaloblasts) appear in the blood
- erythropoiesis = cell division & daughter cells are smaller than parent cells = not much time to become enlarged
- DNA & RNA synthesis is reduced = delaying cell division
- cells grow larger than normal between cell divisions
- circulating cells are immature and larger than normal, and some are nucleated
47
PERNICIOUS ANEMIA
- The most common form of Vitamin B deficiency
- autoimmune disease, antibodies destroy the intrinsic factors (IF) of the gastric parietal cells
- autoimmune disorders, particularly thyroid disease = are more common in the elderly
48
DIETARY DEFICIENCY OF VITAMIN B12
- animal-driven foods = dairy products, meat and eggs
- more common in vegans
- The liver stores vitamins
49
OTHER CAUSES OF VITAMIN B12 DEFICIENCY
> Gastrectomy: leaves fewer cells available for IF
> chronic gastritis, malignant diease and ionising radiation: damage the gastric mucosa
> malabsorption: terminal ileum is removed/inflamed
> vitamin cannot be absorbed despite normal IF levels
50
CONSEQUENCES OF VITAMIN DEFICIENCY ANAEMIA
- irreversible neurological damage
- mucosal abnormalities
- glossitis (inflammation of the tongue), they are reversiable
51
FOLIC ACID DEFICIENCY ANEMIA
- causes megalomaniac anaemia identical to vitamin B deficiency, but not associated with neurological damage
due to:
> dietary deficiency, delay in establishing a mixed diet, anorexia, lack of fresh food
> malabsorption from the jejunum caused by celiac disease
> interference with folate metabolism by cytotixic and some anticonvulsant
52
APLASTIC ANAEMIA
- aplastic (hypoplastic) bone marrow faliure
- Bone marrow produces erythrocyte count, leukopenia (low white cell count) and thrombopenia (low platelet count)
- all types of cells are low = conditions called pancytopenia
- inherited
- Autoimmune disease is original
known causes:
> some drugs, e.g. cytotoxic therapy ( reaction to anti-inflammatory and anticonvulsant drugs and some antibiotics
> ionising radiation
> some chemicals
> viral diseases including hepatitis
53
HAEMOLYTIC ANAEMIA
- erythrocyte breakdown beyond normal
- Haemolysis takes place in the liver
- haemolytic anaemias = cause additional symtpoms, e.g. jaundice
54
CONGENITAL HAEMOLYTIC ANAEMIAS
- leads to the synthesis of abnormal haemoglobin and increased red blood cell membrane fragility
- reducing their O2-carrying capacity and lifespan
- sickle cell anaemia and thalassaemia
55
SICKLE CELL DIEASE
- misshapen when deoxygenated = erythrocytes sickle-shaped
- If cells contain a high proportion of abnormal haemoglobin, sickling is permanent
- distorted shape
- Sickle doesn't move smoothly through the circulation
- obstruct blood flow = intravascular clotting, tissue ischaemia, and infarction
- longer-term problems arising = poor perfusion & anaemia:
> celiac disease
> kidney failure
> poor tissue healing
> blood flow to the brain
> Growth delay in children
- increased risk of stroke and seizures in children
Respiratory complications:
> pulmonary hypertension
- individuals must have two copies of the gene
56
THALAMSSAEMIAS
-inherited condition
- excessive synthesis and accumulation of one of the globins used in haemoglobin production
- damage to developing erythrocytes
- life-threatening
- Symptoms = moderate to severe thalassaemia include bone marrow expansion and splenomegaly
- as the production of red blood cells increases, this will correct an anaemia
57
HAEMOLYTIC DISEASE OF THE NEWBORN
- The mother's immune system makes antibodies that enter the baby's red blood cells and destroy them
- The antigen system involved is usually the rheuses system
- mother carriers Rh- but can produce anti-Rh antibodies
- Her immune system reacts and produces neutralising antibodies to her baby's erythrocytes
- These antibodies are produced in the placenta and enter the child and then destroy their red blood cells
- antibody levels of the baby delivered
58
CHEMICAL AGENTS
- substance causes early or excessive haemolysis:
> some drugs (long-term in large doses)
> chemicals encountered in the general or work environment
> microbial toxins
59
AUTOIMMUNITY
- An individual makes antibodies to their red blood cell antigen = haemolysis
- If individuals need a transfusion, they are incompatible when the antibodies in their blood attack the antibodies in the blood transfusion, compared to if they are using the individual's blood type. They are more likely to comply with the blood transfusion.
- Breakdown products of haemolysis lodge in and block the filtering mechanisms of the nephron = the kidney, and failure = triggers multiple blood clots throughout the circulatory system (disseminated intravascular coagulation) (DIC)
60
POLYCYTHAEMIA
- high red blood cell = increase blood viscosity
- slows down blood flow = raising risk of intravascular clotting, ischaemia and infarction
- cardiac function is higher because blood = thicker than usual & heart failure
- erythrocytes may = high because of plasma volume = reduced = polycythaemia
- Polycythaemia occurs when plasma volume is normal
61
PRIMARY POLYCYTHAEMIA
- associated with specific genetic material = interfere with erythropoietin control of erythrocytes number = polycythaemia vera symptoms: itching, tiredness, headaches
62
SECONDARY POLYCYTHAEMIA
- Polycythaemia identified cause may be expected compensatory response in hypoxic situations
- heart failure or heavy smoking = abnormally high erythropoietin levels seen in kidney tumours
63
GRANULOCYTOPENIA
- low numbers of circulating granulocytes = neutropenia
- Granulocytes are neutrophils
- Neutropenia predisposes to infections (sepsis), indicating the presence of active pathogens in the bloodstream
- occur when production rates fall below normal
- extreme shortages = agranulocytosis
- response to inflammation = activated granulocytes engaged in phagocytosis
caused by:
> drugs
> irradiation of bone marrow
> red bone marrow disorder
> severe infections
64
LEUKOCYTOSIS
- increased number of circulating leukocytes
- normal protective reaction in a variety of pathological conditions
65
LEUKEMIA
- malignant proliferation of white blood cell precursors in bone marrow = production of leukocytes
- immature leukemic blast cells crowd out other blood cells formed in bone marrow = anaemia, thrombocytopenia and leukopenia
- leukocytes = immature when released
- immunity is reduced, and the risk of infection increased
66
CAUSE OF LEUKEMIA
- genetically predisposed, triggered by environmental factors = viral infections
- ionising radiation and some chemicals
67
IONISING RADDIAITON
- The DNA of cells may be damaged
- Some might die, others reproduce @ abnormal rates
- leukaemia develop at any time after irradiation
68
CHEMCIALS
- Some chemicals generate mutations in the DNA of the white blood cell precursors in the bone marrow
69
GENETIC FACTORS
- identical twins of leukemia suffers = higher risk than normal of developing the disease = genetic factors invovled
70
TYPES OF LEUKEMIA
ACUTE LEUKAEMIAS:
- sudden onset
- affects poorly differentiated and immature 'blast cell'
- aggressive diseases
- Most of the white cells are immature & abnormal blasts
- bone marrow = packed with large numbers of blasts
- invasion more quickly = bone marrow failure
- haemorrhaging & more susceptibility to infection
2 types:
> acute myeloblastic leukemia (AML) = increases chance with age
> acute lymphoblastic leukemia (ALL) = more likely in people under 20
71
AML
- polycythaemia of myeloblast
- genetic abnormalities found
72
ALL
- common in children
- The cells responsible are B-lymphocytes
73
CHRONIC MYELOID LEUKEMIAS
- leukocytosis (raised leukocyte count)
- crowning leukaemia = crowning the bone marrow with immature and abnormal cells
74
CHRONIC LYMPHOCYTIC LEUKEMIA
- polycythaemia of B-lymphocytes
- less aggressive than CML
- progression = slow & survival times can = 25 years
75
THROMOBCYTOPENIA
- due to reduce rate of platelet production/increased rate of distruction
76
REDUCED PLATELETS PRODUCTION
- production of erythrocytes and leukocytes = reduced
- giving rise to pancytopenia
caused by:
> crowding out of platelets from the bone marrow in bone marrow disease
> ionising radiation: X-ray
> drugs that damage bone marrow
77
INCREASED PLATELET DESTRUCTION
- reduced platelet count = if production doesn't keep pace with the destruction of damaged & worn-out platelets
- disseminated intravascular coagulation
- autoimmune thrombocytopenic purpura
78
AUTOIMMUNE THROMBOCYTOPENIC PURPURA
- triggered by viral infections, i.e. measles
- A feature of this disease is the presence of purpura = haemorrhages into the skin, ranging in size
- platelet counts are very low, three cases of bruising, haematuria and gastrointestinal or intracranial haemorrhaging
- Antiplatelets are formed that coat plates = platelet destruction & removal from circulation
79
VITAMIN K DEFICIENCY
- needed by the liver
- clotting factors and deficiency predisposes to prolonged clotting times
80
HAEMORRHAGIC DISEASE OF THE NEW BORN
- Premature babies = limited stores of vitamin K
- can cause bleeding in the first few months of life
81
DEFICIENCY IN ADULT
- vitamin K = fat soluble
- Bile salt is required in the colon for absorption
- Deficiency may happen in liver disease
- prolonged obstructions of the biliary tract / another disease where fat absorption is impaired
- Dietary deficiency is rare because a sufficient supply of vitamin K synthesised for bacteria
82
DISSEMINATED INTRAVAUSLAR COAGOLATION
- DIC coagulation system is inappropriately activated within blood vessels
- leading to the formation of intravascular clots and fibrin deposition in the tissue
- depletes clotting factors and platelets in the bloodstream = haemorrhaging
- DIC complications of several other disorders:
> infections
> trauma
> premature separation of the placenta
> acute pancreatitis: digestive enzymes are released into the blood
> advanced cancer
> transfusion of large volumes of blood
83
CONGENITAL DISORDER
- Haemophilia A & Haemophilia B are inherited clotting disorders
- deficiencies in 2 clotting factors
- Haemophilia A = deficient factor VIII & Haemophilia B (Christmas disease)
- The genes are present on the X chromosomes
- Faults in the genes reduce clotting factor production
- recurrent bleeding in joints is common = sever pain & long term joint damage
84
VON WILLEBRAND DISEASE
- inherited bleeding disorder
- Von Willebrand factors are needed for clotting
- transports factors in plasma
- levels are reduced and clotting imparied
