Blood Flashcards
Haemolysis
Breaking down of RBCs
Occurs due to incompatibility of blood type
RBCs block vessels and cause tissues to become hypoxic
In extreme cases, we get lysis of RBC and haemoglobin released into the blood
The iron in haemoglobin is extremely toxic to kidney cells
Other symptoms include: hypotension, kidney failure, DIC (bleeding)
Haemolytic syndrome in foetus/new born
1st pregnancy - Protected by the placenta-blood barrier, the mother is not exposed to Rh agglutinogens until the time of childbirth due to placental tearing
2nd pregnancy:
Antibodies cross placental barrier
Born with severe anaemia
Treatment: use anti-Rh γ globulin to mask Rh agglutinogens
4 diseases of blood plasma
Bleeding
Thrombosis
Hereditary angioedema
Complement deficiency
7 diseases of blood cells
Haematological malignancies Sickle cell anaemia Thalassaemia Haemoglobinopathies Leukopenia - decreased number of leukocytes Thrombocytopenia - low platelet count Infectious mononucleosis
Anaemia
Decreased number of RBCs
Leukopenia
Decreased number of WBCs
Thrombocytopenia
Decreased number of platelets
Erythrocytosis
Increased number of RBCs
Leukocytosis
Increased number of RBCs
Thrombocytosis
Increased number of platelets
Causes of bleeding
Injury (acute)
Disease (chronic) - bleeding internally
Low platelet counts (thrombocytopenia - mild)
Coagulation deficiencies (haemophilia - severe)
Vitamin K deficiency
Drugs
Liver disease (although may also cause thrombosis)
Infection/sepsis: disseminated intravascular coagulation
Aneurysm rupture
Causes of thrombosis
Atheroscelerosis - deposition of lipids in areas of the arterial wall
Cancer
Immobilisation
Surgery
Hypercoagulability
Thrombocythaemia (high platelets level) - pooling of blood in lower extremities
Leukaemia
Accumulation of white blood cells in the bone marrow and blood
Bone marrow failure
Decreased RBCs and platelets
Increased WBCs in blood or in advanced disease, decreased white cells (due to BM failure)
Blood hyper viscosity due to increased WBCs causing respiratory or neurological symptoms
Infection if decreased WBC
Tiredness/anaemia
Bleeding
Lymphoma
Affects lymph nodes
T or B lymphocyte neoplasia
Non-Hodgkin or Hodgkin
Hodgkin Lymphoma characterised by Reed-Sternberg cells
Reed-Sternberg cells generally originate from B lymphocytes, which become enlarged and are multinucleate or have a bilobed nucleus
Microcytic anaemia
Pale and small RBCs due to reduced haemoglobin production
Cause of sickle cell disease
Mutation in the Hb b globin gene Glu 6→Val
Polymerisation of Hb, distorting RBC
Widespread in Africa (Carribean), Middle East, India and Med
Sickle caused because proteins folds incorrectly
Effect of sickle cell disease
“Sickling” of RBC (particularly in homozygous disease)
Sickle cell crisis due to blockage of microvasculature
Heterozygosity confers protection against malaria
Homozygous anaemia is extremely dehabilitating
How do we react to vascular trauma?
Vasoconstriction, reduction of blood flow to the area
Platelet activation and adhesion to collagen
Platelet shape change
Granule release - increased local concentrations of:
Platelet activators
Coagulation factors
Vasoconstrictors
Acts to amplify the haemostatic pressure
Primary plug formed and blood loss stopped
Explain secondary haemostasis - consolidation of the haemostatic plug
4 steps
- FVII from the blood binds to TF expressed on the membrane of cells surrounding the blood vessel
- Activated FVII next proteolytically cleaves and activates FX
- FXa then converts prothrombin to thrombin
- thrombin converts fibrinogen to fibrin
6 triggers for induced bleeding
Trauma Surgery Sepsis Aneurysm rupture Drugs (anticoagulants, aspirin) Vitamin K deficiency (mild to severe)
Vitamin K deficiency
Malnutrition
Fat malabsorption
Liver disease (alcoholic cirrhosis)
May occur in newborns (vitamin K injection/tablets for newborns)
Due to Vitamin K Antagonists (VKA: warfarin, acenocoumarol) over-dosage
Associated with (severe) bleeding - Can be reversed by vitamin K administration
Immune thrombocytopenic purpura (ITP)
produces antibodies against their platelets so theres never a high enough platelet count
2 inherited defects in platelet-vessel wall interaction
Von Willebrand syndrome.
Bernard–Soulier syndrome.
2 inherited in platelet - platelet interaction
Glanzmann thrombasthenia.
Congenital afibrinogenemia.
Platelets don’t stick together so no plug
Wiskott-Aldrich syndrome
Defects in platelet granules, secretion and signal transduction
Haemophillia A
F VIII
Haemophilia B
F IV
Thrombosis
Involves the formation of a clot inside the vessel, blocking blood circulation
This causes ischaemia (tissue death), malfunction, pain or swelling in the organ or tissue affected.
Hypercoagulability
Increased tendency to have thrombosis
Stasis
Lack of movement of the blood causing pooling
Trigger for arterial thrombosis
Rupture of the atherosclerotic plaque
Two types of arterial thrombi
- Mural thrombi
2. Occlusive thrombi
DVT and PE
A blood clot that forms in a vein deep in the body usually in the legs
If a part of the blood clot breaks free (called an embolism) it can become lodged in the blood vessels of the lung, causing pulmonary embolism
