Outline Anaemia Flashcards

1
Q

when dooes Anaemia happen

A

when there aren’t enough red blood cells or haemoglobin

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2
Q

what is Erythropoietin

A

the key regulator of red blood cell development

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3
Q

what is Paroxyimal nocturnal haemoglobinuria

A

a haemolytic anaemia primarily caused by reduced formation of C3-convertase

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4
Q

what causes Anaemia

A

a reduced number of red blood cells in circulation, or a decreased amount of haemoglobin in the red blood cells

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5
Q

results of anaemia

A

reduced levels of oxygen delivery to tissues

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6
Q

true or false, Anaemia may be significant before a patient appears pale

A

true

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7
Q

symptoms of anaemia

A

weakness, tiredness, inability to exercise and shortness of breath
In some cases, this can lead to confusion, thirst and loss of consciousness

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8
Q

signs of anaemia

A
Pallor of the conjunctiva especially 
Tachycardia
Glossitis b12 definicineny
Dark urine in haemolytic anaemia
Koilonychia
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9
Q

symptoms of anaemia

A

decreased work capacity, fatigue, lethargy
weakness dizziness, palpitations
shortness of breath esp on exertion
tired all the time
in children decreased IQ poor concentration and sleepiness
rarely headaches tinnitus (hearing shit) and taste disturbance

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10
Q

mor severe anaemia symptoms

A

jaundice spenomegaly hepatomegly angina cardiac failure fever

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11
Q

: Aetiological classification the bone marrow

A

suppression

infiltration

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12
Q

problems with iron

A

defincinecy at bone marrow
excess absorptions
ineffective incorporation into haem

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13
Q

lack of vitamines

A

B6 and 12

Folic acid

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14
Q

anaemia associated with disease in other organs

A
liver 
kidney
reproductive organs
connective tissue
thyroid
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15
Q

haemolysis

A

due to antibioltics
due to drugs
infections

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16
Q

anaemia arising from gene mutation

A

haemoglobinopathy
membrane defects
enzyme defectts

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17
Q

anaemia due to blood loss

A

haemorrhage

trauma eg RTA,stab

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18
Q

Multipotential

A

Regulated by stem cell cytokines (e.g. SCF, IL-3 and TPO) and haematopoietic niches in the bone marrow

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19
Q

Erythroid

A

Primarily regulated by erythropoietin (EPO) and interactions with macrophages

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20
Q

steps from Multipotential

hematopoietic stem cell to Erythrocyte

A

From Multipotential hematopoietic stem cell
to Common myeloid progenitor
to Proerythroblast (Pronormblast)
to Basophilic erythroblast
to Polychromatic erythroblast
to Orthochromatic erythroblast (Normoblast)
to Polychromatic erythrocyte (Reticulocyte)
to Erythrocyte

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21
Q

Conditions affecting specifically erythropoiesis in the bone marrow are described as

A

PRCA pure red cell aplasia (PRCA)

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22
Q

Conditions affecting production of other cell types in addition to RBCs (white cells and platelets) is termed

A

pancytopenia

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23
Q

what is the most common pure red cell aplasia

A

Diamond-Blackfan anaemia,

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24
Q

what is the cause of Diamond-Blackfan anaemia

A

occurs due to reduced proliferation of erythroblasts. This is a rare condition, occurring in ~5 lives births/million.

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25
Q

how is acquired pure red cell aplasia classified

A

primary (idiopathic – where no clear cause can be identified)

secondary (acquired as a result to exposure to a pathogenic agents such as a drug or infection)

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26
Q

Anaemia from changes in the bone marrow congenial

A

Diamond-Blackfan syndrome, congenital dyserythropietic anaemia

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27
Q

Anaemia from changes in the bone Infections

A
viruses:pavovirus B19 
Hepatitis B virus 
Epstein Barr virus 
Mumps 
Cytomeglovirus
HIV

Bacteria:menigococcal
and staphylococcal species

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28
Q

Anaemia from changes in the bone marrow Malignancy

A
solid tumour (such as cancer of the thymus, stomach, breast, lung, thyroid and kidney)
Haematological tumours (leukaemias, lymphomas, myeloma, myelofibrosis, essential thrombocythemia, Waldenstrom macroglobulinaemia
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29
Q

Anaemia from changes in the bone marrow Autoimmune diseases

A

Systemic lupus erythematosus, rheumatoid arthritus and auto-immune haemolytic anaemia, sjogrens symptoms, autoantibodies to red cell progenitors, autoantibodies to Epo, T-cell mediated recognition of red cell progenitors

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30
Q

what does anaemia from changes in the bone marrow lead to aside from red cell aplasia

A

pancytopenia and aplastic anaemia

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31
Q

Anaemia from changes in the bone marrow other causes

A

drugs and chemicals (notably azathioprine, methotrexate, gold, chloramphenicol, recombinant human Epo and co-trimoxazole)
Pregnancy
Severe renal failure

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32
Q

what does Failure of HSCs to self-renew will eventually lead to

A

exhaustion and pancytopenia

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33
Q

Haemolytic anaemias are caused by

A

the premature destruction (reduced lifespan from ~120 days) of functional erythrocytes either by extrinsic or extrinsic mechanisms.

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34
Q

in Haemolytic anaemia, Anaemia will develop if

A

the bone marrow is unable to match the destruction of erythrocytes by production of new cells.

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35
Q

Erythrocyte destruction usually occurs through 2 broadly different reasons:

A
  1. There is nothing fundamentally wrong with the erythrocyte, but they are destroyed by external pathological processes, such as drugs, toxins auto-antibodies or infection
  2. There is something intrinsically wrong with the erythrocyte so it is destroyed. This can be due to damage, absence of certain enzymes or abnormal types of haemoglobin
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36
Q

what are alloantibodies made in response to

A

the immune recognition of foreign erythrocytes that have been introduced via a blood transfusion or due to pregnancy (following the mixing of maternal and foetal blood at delivery)

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37
Q

One example of Alloantibodies

A

is haemolytic disease of the newborn (HDN)

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38
Q

how does Haemolytic disease of the newborn happen in a fetus

A

HDN develops in a foetus, when the IgG molecules produced by the mother pass through the placenta. Among these antibodies are some which attack antigens on the red blood cells in the foetal circulation, breaking down and destroying the cells.

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39
Q

what happens when the haemolytic diseases of the newborn is moderate or severe

A

many erythroblasts (immature red blood cells) are present in the foetal blood.

40
Q

consequences of haemolytic disease of the newborn

A

ranges from mild to very severe, and foetal death from heart failure can occur.

41
Q

when are Autoantibodies are found

A

when a patients’ immune system produces antibodies that recognize their own erythrocytes as foreign and mediate their destruction

42
Q

Idiopathic AIHA accounts for approximately how many cases.

A

50%

43
Q

what are the most common causes Secondary AIHA can result from many other illnesses

A

include lymphoproliferative disorders (e.g., chronic lymphocytic leukaemia, lymphoma) and other autoimmune disorders (e.g., systemic lupus erythematosus, rheumatoid arthritis, scleroderma, crohn’s disease, ulcerative colitis).

44
Q

Drug-induced Auto-immune haemolytic anaemia are rare, which drugs are they caused by caused by?

A

a number of drugs, including α-methyldopa and penicillin

45
Q

Explain, using what happens when the drugs causing Auto immune Haemolytic ananea bind to the macromolecules on the surface of the RBCs how one type of penicilin allergy forms

A

acts as an antigen. Antibodies are produced against the RBCs, which leads to complement activation. This is one type of “penicillin allergy”.

46
Q

Schisocytes and polychromasia

A

Fragments of erythrocytes and larger, blue-tinged reticulocytes

47
Q

nucleated erythrocytes

A

Nucleated erythrocyte

48
Q

Spherocytes

A

Some cells are very small and termed micro-spherocytes

49
Q

Haemoglobinopathies

A

autosomal co-dominant genetic defects resulting in abnormal structure of one of the globin chains of the haemoglobin molecule

50
Q

what is the most common Haemoglobinopathy

A

Sickle cell

51
Q

how does sickle cell come about?

A

due to mutations in the beta-globin gene.

52
Q

how does the abnormal shape of the sickle cell affect its role

A

affects their passage through the circulatory system, their ability to carry O2 and increased haemolysis

53
Q

Sickle cell anaemia can cause what?

A

vaso-occlusive crises (vessel blockage) visceral sequestration crisis, aplastic and haemolytic crises

54
Q

how many molecules of haemoglobin does the erythrocyte contain?

A

640 million haemoglobin molecules

55
Q

where is haemgobin made

A

made in the erythrocyte cytoplasm

56
Q

how is hameoglobin designed

A

designed to absorb O2 from areas of high O2 content (lungs) and release it where O2 levels are low (tissues)

57
Q

what are the two parts of haemoglobin?

A

contain a protein part (globin) and a complex non-protein part (haem)

58
Q

how many globin subtypes are there

A

4

59
Q

which essential micronutrients are required for various steps in regulating erythrocyte function, especially for the metabolism of haem.

A

iron, vitamins B12 and B6 and folic acid

60
Q

why can iron, vitamins B12 and B6 and folic ac deficiency lead to anaemia

A

These micronutrients are obtained in the diet so malnutrition is likely to cause different types of anaemia

61
Q

how can An apparently adequate diet may still lead to disease

A

as essential micronutrients may fail to be absorbed due to abnormalities of the intestines (malabsorption)

62
Q

how can lack of iron directly impacts the amount of O2 that can be transported to the tissues.

A

Each molecule of haemoglobin must have an atom of iron to which O2 can bind to in the lungs

63
Q

what does the blood film look like in Iron-deficiency anaemia

A

Iron deficiency is characterised by hypochromic (pale) microcytes (small)
RBCs seem to be “empty” with a lack of staining in the centre of the cell
RBCs are also significantly smaller (compare the size of RBCs to the white blood cell in the normal film)

64
Q

daily iron requirements of an infant

A

1mg

65
Q

daily iron requirements of adolescent

A

2-3mg

66
Q

daily iron requirements of a menstruating adolescent

A

3-4mg (loses 20-25mg per menstruation)

67
Q

daily iron requirements of an adult

A

2-3mg (loses 20-25mg per menstruation)

68
Q

daily iron requirements of a pregnant lady

A

3-4mg (500-1000mg req overall)

69
Q

daily iron requirements of a lactating lady (this amenhoroea likely)

A

1.5-2.5mg (but also req to repopulate stores)

70
Q

daily iron requirements of a post menopausal female

A

1mg

71
Q

Intestinal factors contributing to reduced iron absorption in the stomach

A
Achlorydria 
Gastric atrophy 
gastritis
Alcoholism
Gastric Carcinoma
72
Q

Intestinal factors contributing to reduced iron absorption

A
Duodentiis
Caeliacs
Ulceration
Crohns
Other inflamatory blowel dieases
Increaased Hepcidin Levels
73
Q

Intestinal factors contributing to reduced iron absorption

A

resection of stomach or UGI and LGI tissue

74
Q

Iron High content

A
Dark-green leafy vegetables
Iron-fortified cereals
Whole grains
Beans
Nuts
Meat
Apricots
Prunes
Raisins
Iron tablets
75
Q

Makes absorption difficult

A
Tea and coffee
Calcium
Antacids 
Proton pump inhibitors (PPIs)
Wholegrain cereals (phytic acid)
76
Q

What is sideroblastic anemia charaterized by?

A

failure of iron to be incorporated into haem in the erythrocyte precursor cells.

77
Q

There are various forms of sideroblastic anaemia that are the consequence of mutations or deletions of genes regulating the expression of key enzymes involved in haem synthesis. A consequence of the failure to incorporate iron into the correct areas what happens?

A

formation of iron-rich mitochondria which surround the nucleus of the erythrocyte precursor as granules. These cells are termed “sideroblasts

78
Q

what is haem

A

a complex molecule synthesized in the cytoplasm and mitochondria of erythrocyte progenitor cells.

79
Q

what are the key regulators of haem production

A

Vitamins B6 and B12/folate

80
Q

Which is most common, B12 Folate or B6 difficenecy?

A

Isolated vitamin B6 deficiency is rare in the absence of drugs, particularly the anti-tuberculosis agent isoniazid. However, B12/folate deficiency is relatively common

81
Q

B12 replacements

A
Meat
Salmon 
Milk 
Eggs
Fortified cereal replacement
Soy products
82
Q

Causes of Vit B12 Folate deficincines ?

A
Malnutrition and Malabosroption
Poverty
Pregnancy
Drugs 
Pernicious Anamia: deficincency of gastric intrinsic factor
Gastrectomy
Small bowel sprue
Fish tapeworm
antacids 
bacterial overgrowth
pancreatitis
83
Q

what is Vitamin B12/folate is essential for in erythrocyte proliferation

A

DNA synthesis

84
Q

what do defienceies cause?

A

reduction in erythropoiesis

85
Q

HB

RBC

MCV

HCT

MCH

MCHC

RDW

A

haemoglobin

red blood cells

mean corpuscular (cell) volume

haematocrit

mean corpuscular haemoglobin

MCH concentration

Red blood cell distribution width

86
Q

3 causes of anaeomia

A
  • Reduced production of erythrocytes
    • Increased destruction of erythrocytes
    • Reduced production/defective haemoglobin
87
Q

what are the key componants iin the correct diagnosis of aneomia

A

Full blood counts combined with blood films and patient histories

88
Q

what are the three groups we divide anamia into?

A

microcytic, normocytic and macrocytic

89
Q

Macrocytic anaemia is caused by

A

Recticulocytis
B12 and Folic Acid Defincinecy
Liver disease
Hypothyroidism

90
Q

High RBC Microcytic anaemia is caused by

A

Thalassemias alpha and beta or combo with other hamoglobin abnormalities

91
Q

Normocytic anaemia is caused by

A
hemolytic anaemias 
bone marrow disorders 
hypersplenism
acute blood loss
anaemias of chronic dieease
92
Q

MCV of macrocytic anaemia is

A

high

93
Q

MCV of Microcytic anaemia is

A

low

94
Q

MCV of Normocytic anaemia is

A

normal

95
Q

Normal or low RBC Microcytic anaemia is caused by

A

Iron defincinecy anaemia
Lead poising
Aneamia of chronic inflammation
Sideroblastic ananmia