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MEH My own decs > Anaemia > Flashcards

Anaemia Flashcards

1
Q

Define anaemia

A

Haemoglobin concentration lower than the normal range

(normal range varies with gender, age and ethnicity so the point at which a patient becomes anaemic depends on those parameters)

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2
Q

Key clinical point about anaemia

A

It is NOT a diagnosis
It is a clinical manifestation of an underlying disease state
It is important to ESTABLISH CAUSE

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3
Q

Symptoms of anaemia (7)

A 
Shortness of breath
Headaches
Angina
Weakness/lethargy
Confusion 
Palpitations
Claudication
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4
Q

Signs of anaemia

A 
Pallor
Tachycardia
Systolic flow murmur
Tachypnoea (fast breathing)
Hypotension
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5
Q

Specific signs associated with the cause of anaemia

A

Koilonychia (spoon nails, iron deficiency)

Angular Stomatitis (inflammation around mouth, iron deficiency)

Glossitis (inflammation and smooth tongue, Vit B12 deficiency)

Abnormal facial bone development (Thalassaemia)

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6
Q

Reasons anaemia can develop (bone marrow)

A

Reduced or dysfunctional erythropoesis
Abnormal Haem synthesis
Abnormal globin chain synthesis

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7
Q

Reasons anaemia can develop (RBC)

A

Abnormal structure
Mechanical damage
Abnormal metabolism

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8
Q

Reasons anaemia can develop (removal)

A

Excessive bleeding

Increased removal by reticuloendothelial system

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9
Q

Reduced/dysfunctional erythropoesis reasons explained (5)

A

Lack of erythropoietin (chronic kidney disease as kidney produces it)

Bone marrow cannot respond to erythropoietin (eg after chemo)

If marrow is infiltrated by cancer cells or fibrous tissue (myelofibrosis), the number of normal haemopoeitic cells is reduced

Anaemia of chronic disease = no iron available to marrow for bc production

Myelodysplastic syndromes (rare forms of blood cancer) = abnormal clones of stem cells so no capacity to make RBC or WBC

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10
Q

Role of erythropoetin

A
  • It works in a negative feedback loop
  • Pericytes in kidney detect low O2 of blood (hypoxia)
  • Kidney produces erythropoietin
  • EPO binds to receptors on erythroblasts in bone marrow and stimulates RBC production
  • Number of RBC increases
  • High blood oxygen
  • This is sensed by the kidney and EPO production goes down
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11
Q

What is defect in haem pathway called?

A

Sideroblastic anaemia

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12
Q

Reasons haemoglobin synthesis can be affected

A

Sideroblastic anaemia
Iron deficiency anaemia
Anaemia of chronic disease - results in a lack of functional iron
Mutations in genes encoding gloin chain proteins ( we see that in patients with a and b thalassaemia and sickle cell disease)

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13
Q

Inherited reasons for haemolytic anaemia

A
  • Mutations in genes coding for proteins in membrane and cytoskeleton of RBC
  • Cause cells to be less deformable and more fragile
  • They break up in circulation and removed by RES

= haemolytic anaemia (eg Hereditary spherocytosis)

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14
Q

Acquired reasons for haemolytic anaemia

A

Microangiopathic haemolytic anaemia (MAHA) from mechanical damage

Heat damage from severe burns

Osmotic damage (drowning in fresh water)

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15
Q

Reasons for mechanical damage in patients with MAHA (Microangiopathic haemolytic anaemia) occurs

A

Shear stress as cells pass through defective heart valve

Cells snag on fibrin strands in small vessels where clots have been formed and they break down (eg in Disseminated Intravascular Coagulation)

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16
Q

Blood film blood cells mechanical damage

A

Schistocytes - fragments of RBC resulting from mechanical damage

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17
Q

Causes of defect in RBC metabolism

A

G6PDH deficiency

Pyruvate kinase deficiency

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18
Q

Why does G6PDH deficiency cause anaemia?

A
  • Mature RBC’s don’t have mitochondria to give energy, they rely on certain glycolytic pathways
  • Decreased G6PDH = Lack of NADPH
  • Lack of NADPH = lower GSH (glutathione)
  • lower GSH = less protection of RBC from oxidative stress
  • Oxidative stress
  • Oxidative stress (eg from infection, drugs like anti malaria, and broad beans)
  • Oxidative stress leads to
    Lipid peroxidation (leads to cell membrane damage) and protein damage to RBC
    =
    Heinz bodies (aggregates of cross linked haemoglobin)
    Red cells recognised by RES as defective and removed
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19
Q

Why does pyruvate kinase deficiency cause anaemia?

A
  • RBC have no mitochondria so depend on glycolysis for energy production
  • Pyruvate kinase is final enzyme of glycolysis
  • Some patients may have rare genetic defects in this enzyme
  • A defective glycolytic pathway causes RBC’s become deficient in ATP and undergo haemolysis
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20
Q

What are the 3 excessive bleeding causes of anaemia?

A
  • Acute blood loss
  • Chronic NSAID’s (Nonsteroidal anti-inflammatory drugs)
  • Chronic bleeding (most common)
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21
Q

Acute blood loss causes of anaemia

A

Injury
Childbirth
Surgery
Ruptured vessel

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22
Q

Chronic excessive bleeding causes of anaemia

A
  • Heavy menstrual bleeding
  • Repeated nosebleeds
  • Haemorrhoids
  • GI bleeding (blood loss in stool)
  • Kidney/bladder tumours (blood loss in urine)
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23
Q

Causes of GI bleeding

A 
Ulcers (stomach or intestine)
Polyps in large intestine
Intestinal cancer 
NSAIDS
Diverticulotis
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24
Q

How can NSAID usage lead to anaemia?

A

Nonsteroidal anti-inflammatory drugs treat conditions with pain and inflammation:

  • Asprin
  • Ibruprofen
  • Naproxen

They Induce GI bleeding by:

  • Inhibit cyclooxygenase activity
  • Direct cytotoxic effects to epithelium
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25
Q

Describe the role of the Reticuloendothelial system in causing anaemia and

Describe what happens in autoimmune haemolytic anaemias

What can occur as a result of haemolytic anaemias?

A

Haemolytic anaemia = RBC destroyed more quickly due to abnormality or damage

Autoimmune haemolytic anaemia:
- Autoantibodies bind to RBC membrane proteins causing them to be recognised by macrophages in spleen and destroyed

(splenomegaly often occurs with haemolytic anaemias as the spleen is doing extra work)

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26
Q

In haemolytic anaemias, blood cells are destroyed more quickly as they are abnormal or damaged. Where can the damage occur?

A
  • Within the blood vessels (intravascular haemolysis)

- Within the RES (extravascular haemolysis)

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27
Q

Organs involved in RES

A

Spleen

Liver

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28
Q

Myelofibrosis explained

A
  • Mutated haemopoetic stem cells results in reactive bone marrow fibrosis
  • Fibrotic marrow with little space for haemopoesis
  • Mutated Progenitor cells from marrow then colonise liver and spleen leading to extramedullary haemopoesis

(such patients often have hepatomegaly
and splenomegaly)

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29
Q

Thalassaemia explained

A
  • Inherited disorder
  • Results from Decreased/absent alpha and beta globin chain production
  • Results in defective Microcytic and hypochromic RBC

(can result in splenomegaly if haemoglobin H disease)

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30
Q

How to work out the cause of an anaemia/evaluate it

A

1) Size of RBC - macrocytic, microcytic, normocytic (big, small or normal)
2) Presence/absence of reticulocytes - is there a reticulocytosis or not? (is bone marrow responding to anaemia by pumping out immature cells?)

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31
Q

What are reticulocytes?

A

Immature RBC
No nucleus
Take about 1 day to mature into erythrocytes
Slightly larger than mature RBC

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32
Q

What do you bear n mind when measuring MCV?

A

Reticulocytes are Larger than RBC so an increase in reticulocyte number can increase MCV when measuring

33
Q

What do reticulocytes show?

A

If marrow is able to respond to anaemia (you would expect increased reticulocyte count if marrow was responding to anaemia/working normally)

34
Q

Evaluate the Causes of anaemia if the reticulocyte is high/increased

A

1) If there is an increased in reticulocyte count, the Bone Marrow if functioning normally
2) Is there evidence of Haemolysis? (we would know because there would be high bilirubin and high LDH - lacate dehydrogenase)

If YES, determine the cause of Haemolysis:
Autoimmune, MAHA, Membrane defects, enzyme defect, haemonoglobinopathies

3) If no, look for evidence of bleeding:

Acute blood loss
Chronic bleeding
Use of NSAID’s

35
Q

Evaluate the Causes of anaemia if the reticulocyte is low/no increase

A

1) If the reticulocyte is low/no increase, there is a problem in the bone marrow
2) We look at the RBC indices/MCV - Mean cell volume

Microcytic: TAILS
Thalassaemia
Anaemia of chronic disease
Iron deficiency 
Lead poisoning
Sideroblastic anaemia 
Macrocytic:
Vit B12 deficiency
Folate deficiency
Liver disease
Alcohol toxicity
Myelodysplasia

Normocytic:
Could be because they have got a combo of microcytic and microcytic cells
Primary bone marrow failure (e.g. aplastic anaemia)
Secondary bone marrow failure (HIV)

36
Q

Macrocytic anaemia types

A

Megaloblastic
Maconormoblastic
Stress erythropoesis

37
Q

Megaloblastic macrocytic anaemia

A
  • The reticulocyte count is low but the cells are large
  • Interreference with DNA synthesis during erythropoeisis and nucleus isn’t maturing at the same rate as cytoplasm
  • Cell division is delayed and erythroblasts continue to grow to form megaloblasts
38
Q

Megaloblastic macrocytic anaemia causes

A

Vit B12/Folate deficiency

Drugs that interfere with DNA synthesis (anti-cancer)

39
Q

Macronormoblastic macrocytic anaemia

A

Normal nucleus and cytoplasm relationship

Cells just larger than normal

40
Q

Macronormoblastic macrocytic anaemia causes

A

Liver disease

Alcohol toxicity

41
Q

Stress erythropoesis

A

High reticulocyte count

High levels of erythropoetin = accelerated erythropoesis

42
Q

Causes of stress erythropoesis

A

Recent blood loss from haemorrhage

Recovery from haemolytic anaemia

43
Q

Megaloblasts appearance

A

Larger than normal erythroblasts

Large immature nuclei

44
Q

What is folate synthesised from?

A

Bacteria and plants

45
Q

Where is folate found?

A

Animal and veg food

Particularly LEAFY GREENS

46
Q

Where is folate absorbed

A

Duodenum and jejenum

47
Q

What happens to folate when absorbed?

A

Coverted to tetrahydrofolate by intestinal cells

Then taken up by liver - acts as a store

48
Q

Role of folate

A

Provides carbons for other reactions

Synthesis of nucleotide bases for DNA and RNA synthesis

49
Q

Store of folate in body

A

3-4 months

50
Q

Causes of folate deficiency

A

Poor diet

Increased requirements - pregnancy, haemolytic anaemia, severe skin disease (psoriasis)

Disease of duodenum or jejunum (coeliac, crohns)

Drugs that inhibit dihydrofolate reductase (Methotrexate)

Alcoholism

Liver disease/Heart failure

51
Q

Symptoms of folate deficiency

A 
Anaemia symptoms
Reduced sense of taste
Diarrhoea
Numbness and tingling in hands/feet
Muscle weakness 
Depression
52
Q

Key point babies and folate

A

Need 400 micrograms per day of folate before conception to 12 weeks of pregnancy

Deficiency can result in neural tube defects for babies

53
Q

Vitamin B12 function

A

Water soluble
Co-factor for DNA synthesis
Needed for erythropoesis
Normal function and development of CNS

54
Q

What produces Vitamin B12

A

Bacteria (found in foods of animal origin)

55
Q

Vitamin B12 sources

A 
Meat
Fish
Eggs
Milk
Cheese
Yeast extract
56
Q

Vitamin B12 supplements

A

People on vegan diet need to eat foods with fortified B12 or 10 micrograms a day supplements

57
Q

What does vitamin b12 bind to in stomach

A

Haptocorrin

58
Q

What happens to haptocorrin vitamin b12 complex?

A

Digested by pancreatic proteases

Releasing B12

59
Q

What does the released B12 then bind to?

A

Intrinsic factor

60
Q

What does intrinsic factor vitamin B12 complex bind to?

A

Cubam receptor

= receptor mediated endocytosis into enterocytes

61
Q

How does vitamin B12 exit basolateral membrane?

A

Through MDR1

62
Q

How is Vitamin B12 transported in blood?

A

Binds to transcoalbumin

63
Q

Where is B12 stored?

A

Mostly liver - 3-6 years worth of storage

64
Q

Causes of Vitamin B12 deficiency

A

Dietary deficiency (vegan)

Lack of intrinsic factor - Pernicious anaemia

Disease of ileum (Crohns)

Lack of transcoalbumin (congenital)

Chemical inactivation of B12 (nitrious oxide gas use)

Parasitic infestation (tapeworm traps B12)

Some drugs chelate Vit B12 (hypercholestrolaemia drug Cholestyramine)

65
Q

What is pernicious anaemia?

A

Decreased/absent intrinsic factor causing low Vitamin B12

Autoimmune disease

66
Q

Antibodies involved with pernicious anaemia

A

Blocking Ab blocks binding of B12 to IF

Binding Ab prevents receptor mediated endocytosis

67
Q

Symptoms of Vit B12 deficiency

A 
Anaemia
Glossitis / mouth ulcers
Diaarrhoea
Paraesthesia 
Disturbed vision
Irritability
68
Q

What defieciencies cause defects in CNS

A

Vit B12 - demyelination*
and Folate - neural tube

*which then can cause subacute combined degeneration of the cord

69
Q

What is subacute combined degeneration of the cord?

A

Degeneration of the posterior and lateral columns of spinal cord - need urgent haematologist if neurological involvement

70
Q

Symptoms of subacute combined degeneration of the cord

A

Gradual onset - weakness, numbness and tingling in arms legs and trunk
Progressively worsens
Changes in mental state

71
Q

What does lack of B12 do?

A

Traps folate in methyltetrahydrofolate form
Prevents synthesis of thymidine

B12 and Folate cycles are linked

72
Q

How do Vitamin B12 and folate cause megaloblastic anaemia?

A

Thymidine deficiency
Uracil incorporated instead
DNA repair enzymes detect and repair via excision
Asynchronous maturation of nucleus and cytoplasm

(nucleus doesnt fully mature, cytoplasm matures at normal rate)

73
Q

RBC in folate and Vit b12 deficiency

A

Large red cell precursors
Inappropriate large nuclei
Open chromatin

74
Q

Megaloblastic blood film

A 
Anisopoikilocytosis (varied shape and size)
Tear drop
Ovalocytes
Hyper segmented neutrophils
Macrocytic red cells
  • progressively becomes pancytopenia in B12/folate deficiency
75
Q

Treatment of folate deficiency

A

Oral folic acid

76
Q

Treatment of vitamin B12 deficiency

A

Pernicious: Hydroxycobalamine intramuscular (NOT ORAL)

Other causes: Oral cyancobalamine

77
Q

What can happen at start of treatment of pernicious anaemia?

A

Hypokalaemia - increased K+ requirement as erythropoesis is using it

78
Q

What happens if you blood transfuse someone with vitamin B12 deficiency?

A

High output cardiac failure

Heart has adjusted to low O2 and then is working too hard

MEH My own decs (13 decks)

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