AUTO - B. ANAEMIA-COVERED Flashcards
what is haematology
- blood = major organ/tissue
what is blood made of
- RBCs: gas transport (45%)
- WBCs and platelets: immune and clotting (1%)
- plasma: water, electrolytes, glucose, lipids, drugs, plasma proteins etc (60%)
albumins: transport, colloidal osmotic pressure
globulins: transport, clotting, precursors to hormones, defense
fibrinogen: clotting
serum is coagulated plasma (blood plasma without the clotting factors)
RBCs
- no nucleus
- contain haemoglobin for oxygen/carbon dioxide transport
- 120 days lifespan (short)
- fewer RBCs, less iron so can’t transport oxygen as well throughout body = anaemia (fatigue)
synthesis of RBCs
- controlled by erythropoietin (EPO) = polypeptide hormone
- released by peritubular cells in kidney in response to hypoxia
anaemia
at altitude
COPD - EPO converts stem cells to RBCs
- renal disease = loss of EPO - renal anaemia
- recombinant EPO used
Iron
- iron recycled (90%) from breakdown of RBCs in liver and spleen
- but need iron from diet to replace 10%
- iron uptake from GIT increased when iron deficient
excess bleeding
WBCs
- neutrophils (70%) - phagocytosis of microorganisms
- eosinophils (4%) - inflammation
- basophils (0.5%) - release histamine
- monocytes (6%) - phagocytic
- lymphocytes (B and T cells) (33%) - antibodies
Platelets (thrombocytes)
- cellular fragments
- non-nucleated
- clot formation (co-aggulation)
Blood counts
Measures
- RBCs/volume
- WBCs/volume
- haemoglobin (g per volume)
- mean corpuscular volume
- platelets/volume
- haematocrit (packed cell volume) - % that is RBC, dilution of blood causes decreased % (male - 40-52%, female - 36-48%)
- identify anaemias or infections
Mean corpuscular volume
- mean size of RBCs
- microcytic anaemia: small (XS bleeding)
- macrocytic anaemia: large (VitB12 deficiency)
- normocytic anemia: normal
what is anaemia
- reduced levels of Hb
- shortness of breath
- weakness/lethargy
- tachycardia
- nail bed and conjuctiva may be pale (not a reliable sign though) PALLOR
- glossitis (painful red tongue) and angular cheilitis (fissures at corner of mouth) - VIT B12 DEFICIENCY
acute vs chronic bleed
- acute: rapid blood loss (haemorrhage),BP falls
Overtime there is haemodilution
so body compensates for decrease in BP by increasing fluid content in plasma
leading to dilution of RBCs as not enough RBCs so haematocrit decreases - chronic: long term bleeding (gastric bleeding, excessive menstruation)
Treatment
- find and treat underlying cause
- oral iron (FeSO4) - constipation
- prophylaxis in pregnancy - oral iron
- transfusion (blood with more iron)
pregnancy
- dilution and/or iron deficiency (increased demand for blood and iron to baby - microcytic)
- may be normocytic as pregnancy increases MCV but iron deficiency decreases MCV
iron deficiency anaemia
- iron needed for Hb
- microcytic anaemia
caused by
- poor diet
- increased demand eg - pregnancy
- increased losses eg - menstruation
- GI bleeding: ulcers (NSAIDs) and colon cancer patients (50% present with anaemia)
renal anaemia
- complicated chronic kidney disease
- loss of EPO so decreased production of RBCs and Hb levels
- normocytic anaemia
- Fe and EPO
megaloblastic anaemia
- abnormal RBC maturation: large, immature RBCs (megaloblasts)
- impaired DNA synthesis
- macrocytic
symptoms
- anaemia
- jaundice due to breakdown of Hb, RBC not maturing and getting broken down easier and bilirubin produced, so XS Hb
causes
- vit B12 or folate deficiency (produce DNA)
- vegans at risk (B12 from animals)
- lack of intrinsic factor required for uptake of B12 (pernicious anaemia)
pernicious anaemia
- lack of intrinsic factor for absorption of B12 due to autoimmune disease
- treat with vit B12 (hydroxocobalamin IM) - can’t give orally as don’t have intrinsic factor to help absorption of vit B12 so bypass we bypass GIT
- Crohn’s - malabsorption of B12, folate, iron
haemolytic anaemias
- increased rate of RBC destruction
- genetic: abnormal reduction in RBC membrane protein (spectrum) so cells fragile
- acquired: malaria, drug induced
sickle cell anaemia
- caused by SCD: genetic - SNP, change in genes produces abnormal Hb)
- abnormal Hb, insoluble forms crystals at low oxygen so RBC form sickle shapes and may block microcirculation (thinner, longer and don’t carry around as much oxygen)
- leads to haemolytic anaemia
- african/carribean background
aplastic anaemia
- insufficient production of RBCs, WBCs and platelets (pancytopenia)
- problems with stem cells in bone marrow (side effect of anti-cancer drugs)
- decreased resistance to infections, increased bleeding, increased tiredness
- mostly acquired: viral, radiation, drugs (cytotoxic)
treatment:
- bone marrow transplant (tissue match)
- immunosuppressants (to prevent destruction of stem cells)
- colony-stimulating factors (to increase WBC count)
polycythaemia (opposite to anaemia)
- increased Hb content and haematocrit
- increased blood viscosity - poor tissue perfusion
signs and symptoms
- ruddy appearance (redness of cheeks due to increased blood flow)
- cyanosis - blueing of toes and fingers (greater deoxygenation)
- headaches (decreased blood flow to brain)
- blurred vision
- hypertension (increased pressure in system)
caused by
PRIMARY
- changes in bone marrow, stem cell defect - cancer? increased production of RBCs caused by stem defect
SECONDARY
- increased EPO due to altitude, smoking, renal carcinoma
treatment for primary
- venesection (bleeding)
- radioactive phosphorous - myelosuppression (bone marrow suppression
- cytotoxic agents - myelosupression
