1. Fatigue, headaches, faintness 2. Breathlessness 3. Angina 4. Intermittent claudication 5. Palpitations

1. AT into duodenal epithelial cells via HCP1 and incorporated into Ferritin

Anaemia Flashcards by Neil Srivastava

How does a reduction in plasma volume effect Hb levels + when is this situation seen

Increases them

Dehydration

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What are the three types of anaemias

Hypochromic (low MCV)
Normochromic (normal MCV)
Microcytic (high MCV)

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Why may some patients be asymptomatic for anaemia

Slowly falling level of Hb = compensation as oxygen-dissociation curve will shift to the right, so that oxygen is more easily dissociated from Hb

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Symptoms of anaemia

Fatigue, headaches, faintness
Breathlessness
Angina
Intermittent claudication
Palpitations

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How does anaemia additionally effect older people

Exacerbates cardiorespiratory problems

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Clinical signs of anaemia

Pallor
tachycardia
Systolic flow murmur
Cardiac failure

SPECFIC:

Koilonychia (spoon-shaped nails in longstanding iron deficiency anaemia)
jaundice (haemolytic anaemia)
Leg ulcers (associated with sickle cell)
Bone deformities (thalassaemia)

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Investigations for anaemia in peripheral blood

1, Red cell indices

the WCC
Platelet count
Reticulocyte count (indictes marrow activity)
Blood film

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What should be seen on a blood film for anaemia

Two populations of red cells are seen - dimorphic

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How is bone marrow investigated in anaemia

Cellularity of marrow
Type of erythropoiesis
Infiltration of marrow
Iron Stores

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RBC lifespan

120 days

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How does reticulocyte count correlate with bone marrow production measurement

Low count - Production of Bone marrow is an issue

High count - removal of bone marrow is an issue

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What is MCV

Average volume of RBCs

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What is the main cause of anaemia

Iron deficiency
Anaemia caused by chronic disease
Thalassaemia

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What is the average intake of iron

15-20mg

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How much of ingested iron is absorbed by the duodenum

10%

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How is Iron absorbed

AT into duodenal epithelial cells via HCP1 and incorporated into Ferritin

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What happens to absorbed iron so it can travel in th blood

Bound to transferrin -> bone marrow to be incorporated into new erythrocytes

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Where is iron stored in th body

Reticuloendothelial cells as FERRITIN or HAEMOSIDERIN (macrophages in bone marrow, liver and spleen)

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Causes of iron deficiency anaemia

Menorrhagia
GI bleeding
Hookworm (leading cause - GI blood loss)
Poor diet
Malabsorption

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What happens to RBCs in iron-deficiency anaemia

Crucial for haemoglobin production + reduction in iron = decrease in haemoglobin + smaller RBCs

MICROCYTIC ANAEMIA

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Clinical presentation of iron-deficiency anaemia

Brittle nails + hairs
Koilonychia
Atrophy of the tongue papilla
Cheilosis (ulceration of mouth corners)

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What are three differential diagnostics for iron-deficiency anaemia

Thalassaemia
Sideroblastic anaemia
Anaemia of chronic disease

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How is iron-deficiency anaemia diagnosed in blood tests

RBCs and microcytic and HYPOCHROMIC (pale)
Poikilocytosis (variation in shape) and anisocytosis (variation in size)
Serum iron is low
TIBC (total iron-binding capacity) rises to normal (transferrin below 19% saturation = iron deficiency)
5

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How does serum ferritin help in diagnosis

Level reflects amount of iron stored - confirms DIAGONSIS

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What happens to the number of transferrin receptors in iron-defiiceny anaemia

Increases

Reticulocyte in iron deficiency anaemia

Low

How is Iron deficiency anaemia treated

1. Oral Iron (FERROUS SULPHATE)

Side effect of ferrous sulphate

Nausea Abdominal Discomfort Diarrhoea/constipation Black stools

What can be given as a replacement to serous sulphate if side effects are bad

Ferrous GLUCONATE

In extreme cases (e.g. severe iron malabsorption) what can be given

Parenteral iron

What is anaemia of chronic disease

Anaemia that is secondary to chronic disease = anaemia

RBC appearance in chronic disease anaemia

NORMOCYTIC (could be microcytic)

When can RBCs be microcytic in CDA

Rheumatoid and crohn's disease

What is the most common anaemia in hospital patients

CDA

What chronic infections cause anaemia

1. TB 2. Crohn's 3. Rheumatoid 4. SLE 5. Malignancy

Pathophysiology of CDA

1. Decreased release of iron from bone marrow to developing erythroblasts (before they become reticulocytes) 2. Inadequate erythropoietin response (cytokine which increases RBC production) to anaemia 3. Decreased RBC survival

Clinical presentation of CDA

1. Fatigue 2. Headache 3. Dyspnoea 4. Angina 5. Anorexia 6. Intermittent Claudication 7. Palpitations

Level of iron and TIBC in CDA

1. LOW TIBC and SERUM IRON

Level of serum ferritin in CDA

Normal/ raised due to inflammatory process

Level of transferrin receptors in CDA

Normal

Appearance of RBCs in blood count

1. NORMOCYTIC 2. MICROCYTIC 3. HYPOCHROMIC

How is CDA treated

Erythropoietin is effective in raising Hb levels

Side effect of treating with erythropoietin in CDA

Flu Hypertension Rise in platelet count thromboembolism

Main causes of normocytic anaemia

1. ACUTE blood loss 2. CDA 3. Endocrine disorders 4. Renal failure 5. Pregnancy

Clinical presentation of normocytic anaemia

1. Fatigue, headaches, faintness 2. Dyspnoea 3. Angina 4. Anorexia 5. Intermittend claudication 6. Palpitations

B12 and folate levels in normocytic anaemia

Normal

Reticulocyte level in normocytic anaemia

Raised

Hb level in normocytic anaemia

Low

Appearance of RBCs in blood count

NORMOCYTIC

How is normocytic anaemia treated

1. Improve diet with vitamins | 2. Erythropoietin injections

What can macrocytic anaemia be divided into

Megaloblastic | Non-megaloblastic

What is megaloblastic macrocytic anaemia

Presence of erythroblasts with delayed nuclear maturation because of delayed DNA synthesis - large megaloblastic cells with no nuclei

What is non-megaloblastic macrocytic anaemia

Erythroblasts are normal

Main causes of megaloblastic macrocytic anaemia

1. B12 deficiency | 2. Folate deificnecy

What is B12 also known as

Cobalamin

Non-megaloblastic causes of macrocytic anaemia

1. Alcohol 2. Liver disease 3. Hypothyroidism 4. Haemolysis 5. Marrow failure 6. Marrow infiltration 7. Myeloma

What kind of anaemia is pernicious anaemia

Megaloblastic

Where is B12 found

Meat Fish Dairy

Is B12 found in plants

How long are body stores of B12

4 years

How is B12 absorbed

Binding to intrinsic factor produced by parietal cells

Where is B12 absorbed

Terminal ileum

What is B12 needed for

Thymidine and DNA synthesis

Pathophysiology of pernicious anaemia

Impairment of DNA synthesis = delayed nuclear maturation Large RBCs + decreased RBC production in marrow

Why is bone marrow most effected in pernicious anaemia

As its most active in terms of cell division

Why is pernicious anaemia autoimmune

1. Parietal cells are attacked = atrophic gastritis + loss of intrinsic factor production + B12 malabsorption

What age group does Pernicious anaemia effect

Elderly

Risk factors for pernicious anaemia

1. Female 2. Elderly 3. Fair-heard, blue eyes 4. Blood group A 5. Addison's disease + thyroid

Specific diagnosis for pernicious anaemia

Intrinsic factor antibodies in blood tests

In what proportion of patients can intrinsic factor be found in

50% of patients

Signs of pernicious anaemia

1. Parietal and chief cells replaced by mucin-decreting cells 2. Autoimmune gastritis affecting funds with plasma cell + lymphoid infiltration 3. Achlorhydria (reduced HCL production) + absent of intrinsic factor secretion 4. Parietal cell antibodies in serum

Clinical presentation of pernicious anaemia

1. Normal symptoms for anaemia 2. Lemon-yellow skin colour Red sore tongue + cheilosis

Why is skin yellow in pernicious anaemia

Caused by ex ess breakdown of haemoglobin (body will try to remove large RBCs that are defective)

Neurological features of pernicious anaemia

1. Symmetrical parasthesia in fingers and toes 2. Weakness + ataxia 3. Paraplegia 4. Dementia / hallucinations and optic atrophy from B12 deficiency

When do neurological symptoms show in pernicious anaemia

Low levels of B12

Appearance of RBCs in blood count of pernicious anaemia

MACROCYTIC

Appearance of microcytes in pernicious anaemia

1. Oval + hyperhsegmented neutrophil polymorphs with 6 or more lobes in nucleus

Serum bilirubin levels in pernicious anaemia

Raised

Why would bilirubin levels in the plasma be raised in pernicious anaemia

As a result of ineffective erythropoiesis + increased RBC breakdown

What happens to Hb count in pernicious anaemia

Low

Reticulocyte count in pernicious anaemia

Low

What is the diagnostic factor for pernicious anaemia

Low intrinsic factor count

How is pernicious anaemia treated

Oral B12 - dietary causes OR IM HYDROXOCOBALAMIN

Role of Hydroxocobalamin

Replenishes B12 stores

Where is folate found

Green veg

Body stores for folate

4 months

Where is folate absorbed

Duodenum

Pathophysiology caused by folate deficiency

Impairs DNA synthesis = delayed nuclear maturation Large RBCs and decreased RBC production in marrow

Why is folate essential in fetal development

Can result in neural tube defects if deficient

Risk factors for folate dificeny anaemia

Elderly Pregnant Alcohol Crohn's or coeliac

Clinical presentation for folate deficiency anaemia

Same as pernicious EXCEPT no NEUROPATHY

How is folate deficiency anaemia diagnosed

Same as pernicious except B12 levels should be the same, folate levels should be LOW

How is folate deficiency treated

Folic acid tablets daily for four months - never without B12

Why can't folate be given without B12

Cause degeneration of spinal cord

What is haemolytic anaemia

Premature breakdown of RBCs, before hitting 120 day lifespan

What happens to haemoglobin in renal tubular cells in haemolytic anaemia

Broken down and deposited in cells as HAemosiderin

Why does shortening red cell survival not equal anaemia all the time

Cause compensated increase in RBC production by bone marrow

What is compensated haemolytic disease

Red cell loss is contained within marrow's capacity for increased output

How does bone-marrow compensate in haemolytic anaemia

Increases output by 6-8 times by increasing proportion of cells committed to erythropoiesis (erythroid hyperplasia) + expanding volume of active marrow Reticulocytes are released PREMATURELY

Characteristics of RBCs in haemolytic anaemia

MACROCYTIC + stain with a light blue tinge on peripheral blood film

Main causes of haemolytic anaemia

1. Hereditary spherocytosis G6PD deficiency B Thalassaemia A Thalassaemia Sick cell disease Autoimmune haemolytic anaemia

Features of haemolytic anaemia

1. High serum unconjugated bilirubin 2. High urobilinogen 3. High fecal stercobilinogen 4. Splenomegaly 5. Bone Marrow expansion 6. Reticulocytosis (more reticulocytes)