anaemia Flashcards

1
Q

What is anaemia in men and women?

A

Female - Haemoglobin levels below 11.5 g/dl

Male - Haemoglobin below 13.5 g/dl

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2
Q

What are the normal ranges for Hb?

A

female - 11.5 - 16.0 g/ dl

Male - 13.5 -18.0 g/dl

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3
Q

What can influence Hb levels apart from anaemia

A

Blood volume
- Giving IV fluids - increase BV - diluting blood - low Hb reading than expected

  • Dehydrated - not been drinking Hb may be higher than expected
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4
Q

Signs of anaemia ?

A
  • Tired
  • Breathless/SOBOE (short of breath on exertion )
    0
  • Headaches
  • Feeling faint
  • Palpitations
    0 not enough Hb to deliver enough 02 body compensates increasing heart rate and respiratory rate)
  • Exacerbates/can precipitate angina or - intermittent claudication (calf pain when walking - sign of osteosclerosis )
  • Pale
  • Tachycardia
  • Cardiac signs
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5
Q

Important note about diagnosing iron deficiency anaemia’s ?

A

Have to exclude malignancy when dealing with iron deficiency anaemia.
- e.g bowel cancer - bleeding into the bowel so Hb dropping.

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6
Q

how is neutropenic sepsis diagnosed?

A

Neutropenia - Decreased neutrophils - below 0.5 x 10^9/L
+ one of these :

  • Fever - > 38 degrees C

any symptoms and/or signs of sepsis,

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7
Q

What is neutropenic Sepsis ?

A

medical emergency - Neutropenia

  • Less neutrophils , more vulnerable to infection. Patients gets an infection —.> body cant fight it off —–> become septic

Side effect of Chemotherapy almost over treatments. Can destroy bone marrow affecting neutrophil production.

G - CSF - Granulocyte colony stimulating factor can given —– stimulate the production of white blood cells from precursors.

Treatment

SEPSIS 6 pathway

          -
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8
Q

erythropoiesis

A
  1. Bone marrow -Pluripotent stem cell
  2. proerythroblast / pronormoblast
  3. eythroblast / normoblast
    ( start to lose organelles , nuclues)
  4. reticulocyte - ( Should be about 2% of circulating red calls - if haemorrhage - should expect higher proportion of reticulocyte due to blood loss) - loss of red cells so bone marrow compensating
  5. Erthyrocyte ( 120 day lifespan
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9
Q

What is Polycthemia ? Types ?

A

polycythaemia / erythrocytosis - Higher levels of red blood cells (than normal)

Can cause Blood clots.

Apparent polycythaemia - reduced plasma, normal red blood cell conc - blood thicker due to reduced plasma

Relative polycythaemia - sim to apparent but cause by dehydration

Absolute polycythaemia - production of too many red cells.

    0  primary polycythaemia - Bone 
        marrow produce too much RBC
                e. g . polycythaemia vera (PV) - mutation in JAK2 gene - can also effect platelets and WBC - levels abnormally high. 

    0 secondary polycythaemia - too 
       much RBC production but caused 
       by underlying condition. 
           (Respiratory conditions e.g COPD  stimulates liver to release more erythropoietin  in response to hypoxia - causes high levels of Hb and RBC.
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10
Q

What causes low release of erythropoietin ?

A

Kidney disease- leads to lower release and not enough —-> not enough RBC produced.

Can give recombinant erythropoietin.

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11
Q

What is needed for RBC production ?

A
  • Hormones
  • Metal
  • iron
  • Vitamins - Folic acid , B12
  • other vitamins.
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12
Q

Classify the different anaemias according to MCV

A

Microcytic - < 80 FL

       - iron defieciency 
       - Thalassaemia 

Macrocytic - > 96 / 100 fl

         - Megaloblastic - Vitamin B12 , folate deficiency 
         - Normoblastic -  Haemolytic anaemia , Haemorrhage , increased reticulocytes. 

Megaloblast are have hyper segmented  nucleus , normoblast - don't) - Normal sized cells - normal MCV -
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13
Q

What is Anaemia of chronic disease?

A

anaemia of inflammation - anaemia that affects people who have conditions which cause inflammation.

very common is hospital patients

  • Kidney disease -reduced erythropoietin
  • Chronic inflammation - Crohns , Rheumatoid arthritis , malignancy , Systemic lupus erythematosus
  • inflammation states - increased hepcidin
    Hepcidin binds to transpoiten in enterocyte membrane. Causes internalisation of hepcidin and degradation. Stop transport of ferritin outside the cell into blood. )
  • Unwell - RBC might survive for full 120 days
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14
Q

What is iron deficiency anaemia ?

A

Reduce iron levels in blood

Causes
0 Increased loss -
heavy periods , colon
cancer , gastric ulcers

      0 Reduced absorption - 
          IBD  , Celiac disease - 
         ( destruction of 
          duodenal cells. ) , 
          reduced gastrc acid -  non - 
          activation of ferri -reductase 
          (reduces fe3 to fe2)
  0 reduced intake - diet 
              - vege/ vegans - high in fe3+ 
                instead of fe2+ - fe3 harder to 
                absorb has to be converted 
                first. 

              - infant - breast milk low in iron       

0 increased demand 
          - pregnancy 
          - child &amp; adolescence 
         (periods of rapid growth)
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15
Q

How is iron absorbed from diet?

A

Duodenal cell

  1. FE3+ , FE2+ diffuse into cell .
  2. HCL activates ferri - reductase which converts fe3+ into fe2+.
  3. ferritin stores FE 2 + until ready for use.
  4. FE2+ diffuses into blood.
  5. Hephaestin converts Fe2+ to FE3+.
  6. FE3+ transported to target tissues by transferrin.
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16
Q

Characteristics of Iron deficiency A ?

A

Microcytic Hypochromic RBC

  • Reduced MCV (below 80 fl)
  • pale colour RBC
  • Poikilocytosis - wrong
    shape
    0 Spherocytes
    0 elliptocytes
  • Anisocytosis - wrong size - lots of different sizes.
17
Q

What you expect blood test and blood smears to show - Iron deficiency Anaemia ?

A
REDUCED 
         0 haemoglobin 
         0 MCV 
         0 serum iron 
         0 serum ferritin - (below 15 mg/ l - confirms diagnosis )

INCREASED
0 total iron binding
capacity (unbound
transferrin in blood)

      0 Red cell distribution width - different sizes 

Blood smear - microcytic and hypochromic

18
Q

NICE classifications of anaemia ?

A

Anaemia is defined as a haemoglobin (Hb) level two standard deviations below the normal for age and sex:
• In men aged over 15years — Hbbelow 130 g/L.
• In non-pregnant women aged over 15years —Hb below 120 g/L.
• In children aged12–14years—Hb below 120 g/L.
• In pregnant women—Hb below 110 g/L throughout pregnancy. An Hb level of 110 g/L or more appears adequate in the first trimester, and a level of 105g/L appears adequate in the second and third trimesters.
• Postpartum — below 100 g/L

19
Q

Treatments of iron deficiency ?

A

Iron deficiency anaemia should be treated with oralferrous sulfate 200mg tabletstwo or three times a day and continuedfor 3 months after iron deficiencyis corrected.
• Haemoglobin levels (full blood count) should be checked after 2–4 weeks to assess the person’s response to iron treatment.
• People should undergo specialist assessment if there is a lack of response (increase of less than 20 g/L in the Hb level) after 2–4 weeks.

(oral ferrous sulfate + orange juice - helps increase absorption. )

0 IV iron - if oral not tolerated

20
Q

Signs of iron Deficiency A ?

A

Fatigue

headaches

pallor - pale

Atrophic glossitis - absence of filiform papillae. - bald tounge.

koilonychia - spoon shaped nails

Tachycardia

angular cheilitis - inflammation of corners of mouth (oral commissures)

dyspnoea

21
Q

iron deficiency A and general bleeding ? - cancer pathway referral ,

A

○ People aged over 60 years with iron deficiency anaemia.
○ Women aged over 55 years withpostmenopausal bleeding.
Urgent referral should be considered for peopleaged under 50 yearswith rectal bleeding.

22
Q

What is Aplastic anaemia and consequences ?

A

Pancytopenia - reduction in all blood cell lines
0 RBC , WBC , platelets

Autoimmune destruction of Hemopoietic stem cells.

reduced RBC -

         0 consequence -  less 
            oxygenation to 
            tissues - heart pumps 
            faster - chest pain, 
            shortness of breath 

-Leukocytopenia - low WBC

    0 consequence - 
     increased risk of 
     infection (sepsis)

-Thrombocytopenia - low platelets

     0 Consequence - 
    - increased risk of 
      bleeding
23
Q

Causes of Aplastic A?

A

Most often idiopathic

  • can be cause by :
           0 radiation / toxins 
           0 Drugs 
                  - anti- seizure 
                  - anti -thyroid 
                  - chemo drugs/ 
                     agents 
                  - anti- thryoid 
                      drugs - 
                     propylthiouracil , 
                     methimazole 
                   - Antibiotics - 
                     chloramphenicol 
                   , sulfonamides. 
             0 Clonal or genetic 
                 mutations
             0 Infectious agents - 
                HIV, Epstein - barr 
                virus (part of 
                herpes family )
24
Q

What is Falconi’s anaemia ?

A

Most common form of Aplastic anaemia

  • Genetically inherited - caused my inheritance of an abnormal gene which results in reduced production of blood cells by bone marrow.
25
Q

Signs of Falconi’s anaemia /

A

Microcephaly - small head

Small stature

Developmental delay

Cafe - Au - lauit - skin lesions - hyperpigmentation.

Hypoplastic thumb - Missing
thumb

26
Q

Symptoms of Aplastic Anaemia ?

A

Fatigue
Pallor

increased risk of infection (recurrent infection)

reduced platelets - increased risk of bleeding 
      - mucosal bleeding 
      - petechiae - red, purple 
      , brown rash on skin - 
        caused by bleeding 
        under the skin.
Increased bleeding time - INR , PT
27
Q

Diagnosis - Aplastic A ?

A

low platelets, RBC , WBC , reticulocyte (indication of problem with RBC production)

High erythropoietin (by kidney) in response to low RBC

Bone marrow biopsy - 
       what is expected ; 
       REDUCED 
       HAEMOPOIETIC STEM 
       CELLS 
      - absence of maligancy , 
        fibrosis 
      - normal cellular 
        morphology
28
Q

Treatment of Aplastic Anaemia ?

A

under 50 - 1st line - stem cell transplant

  1. HLA (human leukocte antigen) matched to sibling donor for bone marrow transplantation
  2. if no match treat with immunosuppressive therapy - Anti- thymocyte globin (atg) and cyclosporine.
  3. if not successful - unrelated donor therapy
  • some doctors for children - if no sibling done go straight to unrelated donor bypass ATG treatment as relapse is common.
    .

over 50 - immunosuppressive therapy

 - cyclosporine and ATG
 - G- CSF (increases haematopoiesis)
 - Glucocorticoids 
  1. No response to ATG & cyclosporine —> unrelated donor therapy
    * if caused by toxin/ medication remove .
29
Q

What is Folate deficiency ?

A

lack of Vitamin B9

cause 
     - anaemia 
     - Neural tube defects - 
      anencephaly (impaired 
      closure of anterior 
       neuropore)
     - spina bifida - imapired 
       posterior neuropore 
       closure
30
Q

What are folate rich foods?

A
  • leady greens
  • citrus fruits
  • grains and cereals
31
Q

Consequence of folic acid deficiency ?

A

0 impaired DNA division-
affects RBC ,WBC ,
platelets (Macrocytic
megaloblastic anaemia )

0 Pancytopenia

(Folic acid needed to) synthesis thymidine (nucleotide base)

0 Glossitis - inflammation of tongue – damage to cells in tongue not replaced as fast as impaired cell division.

Neural tube defects
- Spina bifida

   - Anencephaly 

Build up of Homocysteine (harmful) - increased risk of atherosclerosis & blood clots

(methylated tetrahydrofolic acid ——–> >Vitamin b12 ( cobalamin ). ——-» methyl cobalamin ———&raquo_space; homocysteine (coverts into methionine due to transfer)

——» - means transfer of ch3 - methyl group

Vitamin needed to reduce homocysteine levels

Homocysteine sticks to endothelial cells and attracts interleukins . Attract neutrophils and platelets etc builds up plaque.

32
Q

Diagnosis of Folic deficinecy A?

A
0 Peripheral blood smear 
     - MCV .> 100 fl 
     - Macroctic - 
       Megaloblastic 
     - increased 
       homocysteine 

0 Bone marrow study
- Megaloblastic changes
in RBC precursors.

33
Q

Causes of Folic acid Amaemia ?

A
0 Increased demand 
           - Pregnancy - 2 -3 
             months store of 
             folate used up 
             faster. 

0 Reduced dietary intake
- for longer than 6
weeks

0 Reduced absorption
- Increased alcohol consumption
- medications e.g
Phenytoin
Trimethoprim - anatagonises action of folate by inhibiting dihydrofolate reductase
Methotrexate - antagonist
Sulfasalazine

34
Q

What is ESR ?

A

Erythrocyte sedimentation rate - blood test that measures how quickly erythrocytes (red blood cells) settle at the bottom of a test tube that contains a blood sample.

  • if faster than normal indicates inflammation and possible inflammatory conditions.
Infection
Rheumatoid arthritis
Rheumatic fever
Vascular disease
Inflammatory bowel disease
Heart disease
Kidney disease
Certain cancers

if slower -
-Polycythemia

  • Sickle cell anemia
  • Leukocytosis, an abnormal increase in white blood cells

A moderate ESR may indicate pregnancy, menstruation, or anemia, rather than an inflammatory disease. Certain medicines and supplements can also affect your results. These include oral contraceptives, aspirin, cortisone, and vitamin A.