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IIH > Anaemia > Flashcards

Anaemia Flashcards

1
Q

What is the defintion of anaemia

A

Reduction in haemoglobin (Hb) or red blood cell function

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2
Q

There are different rages for different groups of people. Can you name them?

Like men and women etc

A

Men-> Higher HB level (<130)
Pregnancy
Age
Labs dependent
Altitude

For men androgens stimulate EPO (erthyproptein)

women have a lower haemoglobin when pregnant you expand your plasma so there’s lower haemoglobin

babies have about a few months supply of haemglobin

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3
Q

What can we find in blood

Cells, etc

A
  • plasma proteins
    • electrolytes
    • hormones
    • nutrients
    • Platelets (buffy coat)
    • White cells (buffy coat)
    • red cells (because they are heavier account for 45%)
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4
Q

Describe the structure of erthrocytes and how it affects functions

A
  • Biconcave structure → allows them to squeeze through caparlieis
  • No nucleus → so that they can have as much haemoglobin in it
  • Colour comes from an iron-containing oxygen transport metalloprotein called haemoglobin in the cytoplasm
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5
Q

What is the function of red blood cells

A

they carry o2 and co2

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6
Q

How many days do RBCs live

A

120 days

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7
Q

Describe erthyropoiesis

A

Pronormobolast: large immature cells found in bone marrow (have blue cytoplasm)

Reticulocyte has extruded nucleus but still has RNA so can still make haemoglobin (not possible in erythrocyte)

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8
Q

Describe Haemoglobin

A
  • Iron containing, oxygen-transport protein
  • Hb made up of 4 polypeptide chains
  • (tetramer)
  • 1 x heme molecule per chain
  • 4 binding sites for O2
  • adult haemoglobin has two alpha and two beta,
  • we make a little HbA2
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9
Q

What is the difference between fetal haemoglobin and adult haemoglobin

A

Fetal haemoglobin has two alpha two gamma, whereas adult haemglobin has an alpha and beta haemoglobin

after first 6 months of life fetal gets replaced by adult

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10
Q

What condition to we use fetal haemoglobin for

A

Sickle cell anameia

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11
Q

Can you describe the oxygen dissociation

A

If it shifts right you will readily release

  • why? if you work really hard in the gym, the muscle produces lactic acid,
  • the temperature will rise, and you will produce more CO2
  • so all of that will shift the curve to the right,
  • which means more oxygen will be released into the cells →
  • and haemoglobin is less attracted to the oxygen
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12
Q

What are the symptoms of anaemia

A

Symptoms

  • fatigue
  • breathlessness on exertion
    • because of o2 carrying capacity has decreased
  • palpitations
    • because your heart is working harder to pump more oxygen around your body
  • angina
    • coronary heart, the heart has to go work harder
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13
Q

What are the signs of anaemia

A
  • pallor
    • patients can look a bit green
      • achycardia
    • because the heart is beating faster
  • bounding pulse
  • flow murmur
  • signs of heart failure
    • if it gets worse
  • Kolionchyia
    • when thumb , tips of nail will curve up
    • Angular stomatitis
    • cuts or sore lips
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14
Q

What are the causes reduced production

like the causes of anaemia

A
  • Iron defiency
  • B12 and folate defiency
  • bone marrow pathology (aplastic anaemia, myelodysplasia)
  • Displacement in bone marrow (leukaemia, other cancer, myleofibrosis
  • Chronic disease (renal failure, myeloma, chronic inflammatory conditions
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15
Q

How do people get iron defiencies

causes of iron defiency

A
  • Dietary
  • Malabsorption (celiacs, and chrons)
  • Chronic blood loss (don’t release you’re losing blood over a long period of time
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16
Q

What can cause anaemia due to a lack of b12 and folate

A
  • Pernicious anaemia
  • Alcohol / diet
  • Increased cell turn over
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17
Q

What bone marrow pathologies can cause anaemia

A

Aplastic anaemia
Myleodysplasia

AA: when stem cells get replaced by fat cells, in bone marrow and then you cant make as many red blood cells

M: youre making red blood cells, but they don’t function that well

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18
Q

How does displacement in the bone marrow occur

A

Leukaemia (when you have loads of WBCs you don’t have time of space to make other cells)

Other cancer (go to the bone, they cant make as many blood cells)

Myelofibrosis

Myeloma

Chrnonic inflammatory conditions

Chronic inflammatory conditions
raised inflammatiatoy agents : IL-6 stimulates hepcidin → blocks abosption of iron in the small intestine, and stops iron from escaping the macrophages

Myeloma: malgiancy of plasma cells

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19
Q

Where is iron absorbed in the body

A

Absorbed in duodenum & proximal jejunum in ferrous (Fe2+) state.

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20
Q

In what form do we prescribe iron

A

often prescribe ferrrous sulfate because its in fe2+ form,

Can take tablet with a glass orange juice so it can turn it fe2+

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21
Q

How is iron stored in the body

like what is stored iron called

A

Stored as ferritin

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22
Q

Where in the body is iron formed

A

majority in bone marrow, liver and spleen

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23
Q

Why do we need folate

A
  • Folate is needed to turn uracil into thymidine, an essential building block of DNA

B12 is involved in this process

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24
Q

Where is 95% of the folate in the body stored

A

More than 95 % of folate in the body is in the red blood cells. (we have a short store of folate)

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25
Q

What happens to folate when the body is under stress

A

folate store gets depleted

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26
Q

Where in the body do we store B12

A

Liver

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27
Q

How long can we store B12

A

3-5 years

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28
Q

How long can we store folate

A

about 4 months

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29
Q

What can proudcing excess RBCs do to folate

in haemolysis

A

can cause folate defiency

becasue the rbcs are dying

30
Q

Explain how problems in the GI tract can cause anameia

A

Any inflammation or dysfunction of stomach , duodenum, liver, small or large bowel can cause malabsorption

Eg: Gastritis / colitis Pernicious anaemia / Coeliac disease Gastrectomy / colectomy

31
Q

What is haemolysis

A

breakdown of red blood cells

32
Q

What are the immune reasosn for haemolysis

A

you make antibodies against RBCs,
they stick to RBCs,
and then the macrophage eats it,

33
Q

What are the non immune causes of haemolysis

A

– Splenomegaly (steal RBCs)
– Bleeding

34
Q

What is Hereditary spherocytosis

A

It is when there is a defect in the red blood cell cytoskeleton (spectrin helps keep integrity)

usually there is genetic inherited mutations in spectrin (sometimes other proteins) that makes it go from a biconcave structure to a sphere

Why is that a problem?
it’s the least flexible configuration – gets damaged easily

35
Q

What happens to red blood cells during Hereditary spherocytosis

A

Macrophage is like hey you don’t look like an RBCs,
so the damaged cells get removed by macrophages in the spleen

36
Q

What are the symptoms of Hereditary spherocytosis

A

Symptoms presnet during childhood

Paleness
jaundice
Stomach pai
Shortness of breath
Lack of energy
Lack of appetite
Irritability

but a virus can make symptoms worse

37
Q

What is the treatment of Hereditary spherocytosis

A
  • Folic acid
  • splenectomy
    • complication in terms of infections
  • VERY RARE but can do a transfusion
38
Q

How do we diagnose Hereditary spherocytosis

A

through genetic tests

39
Q

Is Hereditary spherocytosis autsomal or sex linked

and is it dominant or reccessive

A

Autosomal dominant

40
Q

What is thalassaemia and what is the effect in haemoglobin

A

Defect in alpha or beta globin gene

Results in an abnormal form of haemoglobin which presents with anaemia

41
Q

What populations does thalassaemia affect

A

Usually South Mediterranean, north Africa, middle east and SE asia distribution

42
Q

What are the presentations of someone with Thalassaemia

A

dark urine, jaundice, and splenomegaly

43
Q

Find out what haemoglobinopathy ….

A

Haemoglobinopathies are inherited disorders of globin

44
Q

Is Thalassaemia, autosmoal or sex linked

and is it dominant or reccessive

A

autosomal recessive

45
Q

What is beta thalassemia

A

caused by absent or reduced synthesis of beta globulin

Happens in children

46
Q

How can a child inherit beta thalassemia

A

it’s autosomal recessive

you can have asymptomatic carriers, two parents carriers can have a 25% chance of producing a child with beta-thalassemia major

47
Q

If a child has beta thalassemia what treatment options are avaliable

A

the child from a young age will be transfusion-dependent

(gene therapy is being trialed)

48
Q

How can we diagnose HB problems

A

electrophoresis

49
Q

Is sickle autsomal or sex linked

and is it reccessive and dominant

A

Autosomal recessive

50
Q

How can you have sickle cell anaeima and be asymptomatic

A

if you have one beta chain, you are usually asymptomatic

51
Q

In what countries is there a high level of sickle cell anaemia

(and why)

A

High prevalence West / North Africa

(Why: due to protection of malaria)

52
Q

How does having sickle cell anaemia affect RBC

A
  • Defect of Hb beta-globin gene
    • What happens is there is a single amino acid change from Glutamic acid → valine
      • this then Changes the shape of Hb
      • No biconcave shape, so it can obstruct capillaries → They can get stuck and cause painful crises & end organ damage
53
Q

What can be a side effect of sickle cell anaemia

A
  • Hyposplenism
    • they can get a small spleen
    • which can put them at risk of capsule bacteria infections,

To prevent this you can put them on penicillin

54
Q

What is the treatment of sickle cell anaemia

A
  • oxygen, fluids
  • warm them up
  • give them pain killers
  • Exchange transfusion (if hypoxic or have other features like severe crisis)
    • take a pint of their blood and replace it with normal blood
  • Hydroxycarbamide
    • suppresses bone marrow production
    • for sickle cell anaemia, it increases HBf production

Hydroxycarbamide: which is helpful as sickle cells readily gives oxygen, and HBf does the opposite

55
Q

Is G6PD deficiency autosomal or sex linked

A

X linked

So affects men more

56
Q

What will a lack glucose-6-phosphate dehydrogenase (G6PD)

A
  • Important enzyme in pentose phosphate shunt
  • Maintains reduced NADPH = only source of glutathione in RBC
  • glutathione mops up free radicals
    • If you are in a stress-oxidative state then you produce too many free radicals which will cause RBC to haemolyse (break down)
57
Q

At what age do people with G6PD deficiency present?

and what do they present with

A

Present as neonates with neonatal haemolytic anaemia

58
Q

What food do people with G6PD defiency have to avoid and why?

A

AVOID: Fava beans

Why: they produce more free radicals so patients must avoid them. → ‘Favism’

59
Q

What can G6PD cause

A

Acute non spherocytic haemolytic anaemia

causes destruction of RBCs

60
Q

How would you investigate anaemia

A
  • Full history + exam
  • full blood count and film
  • measure ferritin, b12, and folate
  • look at liver (TPO) and kidney function (EPO)
  • Haemolysis screen (is the bilirubin up, are the reticulocytes up, is the LDH up)
61
Q

Full blood count terms

Haemoglobin

A

Concentration of Hb in blood

62
Q

Full blood count terms

Haematocrit

or Packed cell volume (centrifugation)

A

Ratio of volume of red blood cells to the total volume of blood

useful in patients that make too many red blood cells, (too much RBCs, puts them at risk at stroke)

63
Q

Full blood count terms

Red blood count

A

How many red blood cells you have

64
Q

Full blood count terms

Mean cell volume

A

Average red blood cell size

How to calculate = (=PCV/RBC)
Haemrocrit / red blood cell count

65
Q

Full blood count terms

Mean corpuscular hemoglobin (MCH)

A

Amount of haemoglobin per red blood cell

How to calculate= (=Hb/RBC)

66
Q

Full blood count terms

Mean corpuscular hemoglobin concentration (MCHC)

A

The amount of haemoglobin relative to the size of the cell

How to calculate: (=Hb/PCV)

67
Q

How we use HB and MCV to diagnose anaemia

Someone’s FBC shows low HB and Low MCV
What are the potential causes

Low mcv: microcytsois (small red blood cells)

A

Iron defiency
Thalassemia
Sickle cell

68
Q

How we use HB and MCV to diagnose anaemia

Someone’s FBC shows low HB and Normal MCV
What are the potential causes

A

Chronic disease
Acute blood loss
Bone marrow failure

69
Q

How we use HB and MCV to diagnose anaemia

Someone’s FBC shows low HB and high MCV
What are the potential causes

high mcv (macrocytosis) large red blood cells

A

B12 + Folate
Alcohol and drugs
Haemolytic anaemia

70
Q

In summary what the two common causes of anaemia

A

blood loss
- iron deficiency

IIH (7 decks)

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