5. Cardiovascular System Pathologies Flashcards
Anaemia
• A deficiency in haemoglobin given the persons age, sex and geographical location.
Anaemia: Signs and Symptoms
SIGNS & SYMPTOMS:
• Fatigue, shortness of breath on exertion, palpitations, irritability, fainting.
• Signs: Tachycardia, thin & threadypulse, pallor (skin/conjunctiva).
Normal Haemoglobin ranges
Males 13 - 18 g/dl
Females 11.5 - 16.5 g/dl
Pregnanct >11 g/dl
Iron-Deficiency Anaemia
- The most common cause of anaemia worldwide.
- Iron deficiency leads to a reduced concentration of haemoglobin in erythrocytes causing them to appear paler & smaller. Hence iron deficiency anaemia is a ‘hypochromic microcytic anaemia’.
Iron-Deficiency Anaemia: Causes
- Deficient dietary intake (e.g. low dark leafy vegetables).
- Malabsorption (i.e. low stomach acid, coeliac disease etc).
- Excessive blood loss (i.e. from menses/GIT bleed).
- Excess requirements e.g. Pregnancy, rapid growth.
Iron-Deficiency Anaemia: Signs and Symptoms
SIGNS & SYMPTOMS:
• General anaemia signs & symptoms.
• Key signs: Spoon shaped nails(koilonychia), angular stomatitis, glossitis, brittle hair, tachycardia.
• Blood tests:Low RBCs & Hb, low ferritin (correlates with total body iron stores).
Iron-Deficiency Anaemia: Treatment
TREATMENT:
• Treat cause!
• Also: Herbs (Withania), beetroot, dark green leafy vegetables, pumpkin and sunflower seeds. Iron supplementation.
Megaloblastic Anaemia
- Megaloblastic anaemia is characterised by large, immature and dysfunctional red blood cells.
- Folate (folic acid) & vitamin B12 are required for DNA synthesis in all proliferating cells, hence affecting rapidly dividing cells (erythrocytes).
- DNA replication is slowed down and cell growth continues without division and maturation, resulting in large erythrocytes (may have nucleus and has shorter life span) –macrocytic cells.
- Diagnosis by blood test: ‘MCV’>97 fL.
Megaloblastic Anaemia: Causes
- Deficient dietary intake of folate (folic acid) &/or vitamin B12 (rare, except in vegans).
- Lack of intrinsic factor due to autoimmune disease (pernicious anaemia), gastrectomy, chronic gastritis, stomach cancer, coeliac disease.
- Malabsorption in crohn’sdisease, surgical excision.
- Drugs–‘methotrexate’is a folate antagonist.
- In order for folate to function in the body, it must be modified by an enzyme that requires Vitamin B12.
- The liver has abundant stores so if absorption is impaired it takes 2-4 years to develop (folate only 4 months).
Megaloblastic Anaemia: Signs & Symptoms
SIGNS & SYMPTOMS:
• General anaemia signs & symptoms.
• Enlarged red sore shiny tongue.
• Neurological symptoms:Tingling, numbness, weakness, loss of co-ordination, burning sensations, tinnitus, depression (only B12)
Megaloblastic Anaemis: Treatment
TREATMENT:
• Increase Vitamin B12 status OR
• Folate supplementation
Aplastic Anaemias
- A rare and potentially life-threatening failure of haematopoiesis (blood cell production).
- ‘Pancytopenia’ (lack of all three blood cell types) and hypocellular bone marrow (few or no cells).
Aplastic Anaemias: Causes
- Congenital (“fanconi’sanaemia”).
- Idiopathic(unknown cause).
- Can be secondary to drugs (naproxen, diclofenac etc.), chemicals, radiation, cancer, hepatitis/EBV.
Aplastic Anaemias: Signs and Symptoms
• Anaemia (pallor, headache, dyspnoea, palpitations etc).
• Multiple infections (due to low white blood cell count)
• Easy bleeding(due to low thrombocyte count).
Most common cause of death is sepsis, then haemorrhage
Aplastic Anaemias: Treatment
- Treat the cause.
- Bone marrow stem cell transplant.
- Platelet transfusion/blood transfusion.
Haemolytic Anaemias
- Anaemia resulting from excessive breakdown of erythrocytes, when bone marrow activity cannot compensate for the loss of RBC’s.
- Erythrocyte life span can become as low as 5 days.
Haemolytic Anaemias: Causes
- Genetic (e.g. sickle cell, thalassemia).
* Rhesus factor incompatibility, malaria, some drugs, chemicals, autoimmune, radiation.
Haemolytic Anaemias: Signs and Symptoms
- Same general signs & symptoms of anaemia.
- Jaundice (excess bilirubin production).
- Splenomegaly (excess haemolysis in the spleen causes it to enlarge, leading to abdominal distention and a feeling of fullness quickly whilst eating.).
- Gallstones and vascular occlusions.
Sickle Cell Anaemia
- Sickle cell anaemia causes a deficiency of the 2-alpha 2-beta formation of haemoglobin and causes it to sickle up.
- When HbS gives up oxygen to interstitial fluid, it causes the erythrocyte to sickle up.
- These cells rupture easily. Even though erythropoiesis is stimulated, it cannot keep up with the rate of haemolysis.
- The sickle trait protects against malaria because it causes sickle formation and potassium leakage out of erythrocytes.
- Sickle cell is an inherited recessive condition (substitution chromosome 21), affecting African and Caribbean populations.
Sickle Cell Anaemia: Signs and Symptoms
- Usually begins 3-6 months of age as HbFfalls.
- General signs and symptoms of anaemia.
- Splenomegaly and jaundice.
- Can also occlude vessels and cause ischaemic pain: pain in fingers, placental infarction, strokes, renal colic.
Sickle Cell Anaemia: Diagnosis and Treatment
BLOOD TEST:
• FBC and blood film. Hb is 6-8g/dL.
TREATMENT:
• Analgesics (pain relief), fluid therapy, blood transfusion, bone marrow transplant.
Thalassaemia
- Thalassaemia describes a defect in synthesis of either the alpha or beta Hb chains.
- An inherited disease (recessive).
Thalassaemia: Signs and Symptoms
- B-Thalassaemia -> Starts when HbA production begins/gamma chain ceases (usually later part of first year). Causes ‘failure to thrive’ and anaemia.
- A-Thalassaemia -> Can be lethal in utero in severe cases (‘major’). Signs/symptoms of anaemia, jaundice, splenomegaly, hepatomegaly. To compensate haemolysis, bone marrow proliferation (mostly skull/ribs).
Haemolytic Disease of the Newborn
- Occurs when the mother produces Anti-Rhesus antibodies that cross the placenta.
- The antibodies bind to the foetal rhesus antigens, causing agglutination & haemolysis.
- Sensitisation occurs with the first baby producing maternal antibodies against rhesus.
- The greatest possibility of sensitisation occurs at delivery, so the first born child is normally unaffected.
- Anti-Rhesus antibodies can be given during pregnancy to bind to Rhesus antigens and block them.