L.3 Introduction to Anaemia Flashcards
Anaemia signs (5)
- Pallor (especially of the conjunctiva)
- Tachycardia (Pulse rate over 100 beats per minute)
- Glossitis (swollen & painful tongue)
- Koilonycha (spoon nails)
- Dark urine (Haemolytic Anaemia
Anaemia symptoms
- Decreased work capacity, fatigue, lethargy
- Weakness, dizziness, palpitations
- Shortness of breath (especially on exertion)
- “Tired All The Time” (TATT)
- In children: poor concentration & dizziness
Aetiological classification of anaemia (7)
- Problem in the Marrow = Suppression/Infiltration
- Problem in the Peripheral Blood =
Haemolysis / Increased Destruction of RBC’s - Due to Blood Loss =
Haemorrhage / Trauma - Gene Mutation =
Haemoglobinopathy, Membrane Defects, Enzyme Defects - Problem with Iron =
Deficiency in the bone marrow, Excess absorption - Nutritional deficiency =
Vitamin B12 & Folate - Anaemia due to disease in other organs =
Liver, kidney
IDA Lab diagnosis
FBC- Hb, RCC, MCV, MCH, RDW, WBC, Platelets
Hb reduced
RCC reduced
MCV decreased
MCH decreased
RDW = normal or high
WBC = normal or high
Platelets = low, normal, or high.
IDA blood film morphology
Microcytic
Hypochromic
Anisocytosis - progressively abnormal - elliptocytes (pencil-shaped cells), target cells, dacrocytes
Reticulocytes normal or low.
IDA Iron studies ( serum iron/ ferritin/ transferrin/ TIBC)
Serum iron decreased
Serum ferritin decreased (important differentiator ACD and IDA)
Transferrin saturation decreased
TIBC increased
IDA treatment
Oral iron therapy
Blood film of IDA following oral iron medication
Can contains ‘old’ microcytic RBCs as well as ‘new’ normal RBCs.
Anaemia of Chronic disease lab diagnosis
Hb / serum iron/ transferrin saturation / TIBC/ ferritin
Hb slightly low.
Serum iron = low
Transferrin saturation = normal or low
TIBC = normal or low
Ferritin = high or normal
CRP = high
Hereditary Haemochromatosis
Increased absorption of iron from GI tract
Caused by mutation (C282Y) which reduces Hepcidin production leading to increased plasma iron.
25% of irish population have mutation.
HH lab diagnosis
FBC, Iron studies + more
FBC = Hb increased, normocytic, normochromic
Iron studies = serum ferritin v. high, serum iron v. high, transferrin saturation high.
C282Y mutation in PCR
V. strong haemosiderin staining in BM + liver.
HH treatment
Phlebotomy - weekly for 6 months and then 2-4units/year continued indefinitely.
RBCs are ___cytic in IDA because
Microcytic bc Iron availability is decreased => haemoglobin production decreased -> new RBCs contain less Hb = smaller and paler.
Thalassaemia RBCs are ____cytic because
Microcytic = genetic defect in globin chain production leading to imbalanced Hb synthesis = RBCs contain less Hb.
RBCs are ___cytic in anaemia of chronic disease because
First normocytic and can develop to microcytic = 1. Increased hepcidin production (due to inflammatory cytokines IL-6 produced in liver) leading to iron sequestration. Hepcidin blocks ferroportin preventing iron release -> less iron reaches developing RBCs in BM leading to defective Hb synthesis.
2. Decreased erythropoiesis = inflammation suppresses EPO production reducing RBCs -> to maintain Hb concentration, developing RBCs undergo extra divisions, resulting in smaller cells.
Microcytic anaemia (4)
- IDA
- ACD
- Thalassaemias
- Sideroblastic anaemia
Normocytic anaemia (5)
- Acute blood loss
- Early IDA
- Early ACD
- Increased destruction of RBCs
- Bone marrow disorder
Macrocytic anaemia (4)
- Liver disease/alcohol injury
- Metabolic disorder (VitB12/folate deficiency)
- Bone Marrow disorder
- Megaloblastic anaemia
IDA red cell distribution width
HIGH
anisocytosis + poikilocytosis (elliptocytes, targetcells, dacrocytes)
Thalassaemia + Anaemia of CD RDW
Normal
No variation in size and shape
% reticulocyte count in anaemia patients
Misleading because it can be falsely elevated due to patients RBCs being depleted.
%retic is #retic as percentage of # RBCs.
Why is retic count HIGH in thalassaemia?
*In thalassaemia, there is genetic defect in globin chain synthesis leading to ineffective erythropoiesis
*However bone marrow is hyperactive and tries to compensate for defective RBCs by producing more reticulocytes
WHy is retic count LOW in IDA?
- in IDA there is not enough iron available for Hb synthesis so RBC production is limited.
*Cannot increase retic production due to lack of iron.
Why is retic count LOW in ACD?
- In ACD, inflammatory cytokines (IL-6) increase hepcidin which traps iron in macrophages + enterocytes, blocking its release leading to reduced RBC production.
- Inflammation also suppresses erythropoitin (EPO) reducing BM activity.
Absolute reticulocyte count formula
%reticulocyte
——————- x RBCs = ___ x10^9/L.
100
