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Block 34 Metabolic Flashcards > Haematology > Flashcards

Haematology Flashcards

1
Q

What are the indications of blood transfusions

A
  • active bleeding in trauma or surgery or anything else
  • SCD or thalessemia
  • leukaemia

Hb is less than 80 and the patient is symptomatic

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2
Q

What is FFP

A

Frozen plasma

Is done to replace coagulation factors

Can be given in TTP, or to reverse warfarin or severe chronic liver disease

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3
Q

When is platelet transfusion required

A

When platelets are below 50 + active bleeding

Shouldn’t be transfused in patients with TTP or drug induced thrombocytopenia (heparin)

Ocular and neurosurgery

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4
Q

What is cryoprecipitate

A

Used to replace VIII and fibrinogen. After a massive haemorrhage

Or can be congenital fibrinogen deficiency

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5
Q

Transfusion reaction presentations

A

Pruritus
Jaundice
Shock
Renal fialaure
Flank pain
Haemoglobiinuria
Fever
Tachypneoa
Tachycardia
Hypotension

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6
Q

Treatment for AHTR

A

Fluid resus ‘

Correct electrolytes

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7
Q

What is Febrile non haemolytic transfusion reaction

A

No haemolysis occurs and fever occurs due to endogenous release of pyrogens

Give anti-pyretics

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8
Q

Transfusion complications on lungs

A

TRALI - acute noncardiogenic pulmonary oedema within 6 hours of receiving blood products
Neutrophil activation which releases o2 species that damages pulmonary vasculature + extravastion of fluid

  • diuretics not helpful in this as not heart related. Steroids helpful as this is immune mediated and ventilation

TACO - (within 12 hours) patient already has underlying heart failure in which transfusion rate is not adjusted leading to circulatory overload. The heart cannot tolerate this overload which will cause hypertension leading to pulmonary oedema. Raised JVP

Treatment - respiratory support and diuretics

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9
Q

Anaphylactic transfusion reaction

A

Symtoms occur within 4 hours of transfusion

Caused by release of histamine by mast cells

Managed with steroids and fluids?

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10
Q

Septic transfusion reactions

A

Within 4 hours symptoms of sepsis occur

Most common organisms are staph a. And gram negatives

Treat with vancomycin and aminoglycosides

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11
Q

What occurs in vessel injury

A

BV constriction
Platelet activation
Activation of coagulation cascade

Clotting is down regulated by fibrinolysis, Protein C and S, anti-thrombin III

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12
Q

How to differentiate between petechiae, purpura and ecchymosis

A

Petechaie - less than 2mm

Purpura - 2mm to 1cm

Ecchymosis >1cm

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13
Q

Bleeding into deep tissues, joints and muscles suggest what

A

Coagulation factor deficiencies

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14
Q

What drugs can cause thrombocytopenia

A

Amiodarone
Carbamazepine
NSAIDs
Tamoxifen

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15
Q

What is ITP:

A

Autoimmune condition mainly affecting women in which immune system attacks platelets targeting the GP IIb/3a complex. Trapped within the spleen and removed by splenic macrophages

Mild - gums, nose and heavy periods (might cause anaemia)

  • no organomegaly should occur or lymphadenopathy

20-40s age and presents suddenly

Steroids treatment of choice

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16
Q

What is TTP

A

Rare disorder : Pentad

Thrombocytopenia (as platelets are used in making micro-thrombi)
RBC fragmentation
Kidney failure
Neurological dysfunction
Fever

VW protein is released from endothelial cells when required for platelet aggregation. In this disease ADAMTS13 ( a protease which cleaves VW protein when not needed) is deficient meaning lots of VW protein can clump together leading to micro thrombi. Micro thrombi cause micro vascular injury affecting all the above systems within the body. Presence of microthrombi can damage RBC)

Petechaie
Fever
Confusion
Headaches
Coma

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17
Q

What is the normal PT time and what pathway does it measure

A

10 to 14 seconds

Extrinsic pathway

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18
Q

What is normal PTT time and which pathway does it meausre

A

Intrinsic

25-38

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19
Q

What causes prolonged PT time

A

Defieciency in factor 12

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20
Q

Causes of prolonged PTT time

A

Low factor 8,9,10 + 11

Von willebrand disease

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21
Q

Haemophilia A

A

Low factor 8

X-linked

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22
Q

Haemophilia B

A
  • low factor 9

X-linked

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23
Q

What is haemophilia C

A

Low factor 11

Treated by FAP

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24
Q

Role of VW protein

A

Is a glycoprotein that acts to platelet adhesion and helps to carry factor 8

In disease:

Platelet levels are normal, PT normal

PTT is prolonged and VW low. Factor 8 will also be low

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25
Q

What is VW disease treated with

A

Tranexamic acid?

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26
Q

What is the definition of haematocrit

A

Of the centrifuged sample what proportion of the blood is made up of red blood cells

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27
Q

What are the causes of microcytic anaemia

A

Iron deficiency anaemia
Thalessemia
Congenital sideroblastic anaemia
Anaemia of chronic disease
Lead poisoning

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28
Q

What can cause iron deficiency anaemia

A

Menorrhagia
Pregnancy
GIT malignancies
Oesophagitis
GORD
Coeliac disease
Hookworm - and schistosomiasis
Low iron diet - vegans

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29
Q

What is transferrin

A

A protein which is responsible for the transport of iron through out the body

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30
Q

What is ferritin

A

A protein which stores iron

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31
Q

What would the FBC picture look like in microcytic anaemia

A

Microcytic and hypochromic cells

Decreased MCV

Decreased MCH

Decreased ferritin

Decreased iron

Increased transferrin and TIBC

Blood film - anisocytosis (RBC are different sizes) + poikilocytosis (RBC are different shapes).

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32
Q

Causes of normocytic anaemia

A

CKD
Haemolytic anemia
Aplastic anaemia
Anaemia of chronic disease
Acute blood loss
Pregnancy
Hypothyroid

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33
Q

What can cause haemolytic anaemia

A

Glucose 6 phosphate deficiency (enzyme that protects the RBC from oxidative stress and destruction)

Hereditary spherocytosis - Rbc are sphere shaped and more fragile + prone to haemolysis

Haemolytic disease of the newborn

Sickle cell disease

Warm antibody autoimmune haemolytic anaemia - at higher temperatures plasma cells attack RBC causing their destruction - mainly IgG

Cold antibody autoimmune haemolytic anaemia - IgM at lower temperatures attach to RBC causing them to agglutinate and undergo destruction

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34
Q

What are Heinz bodies

A

Most commonly seen in G6P deficiency - when the body detects damaged Hb it tries to remove it from the cell leaving behind a small round blue black body known as a Heinz body

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35
Q

WAIHA is usually associated with what condition

A

CLL

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36
Q

CAIHA is usually associated with which conditions

A

Lymphoma
Mycoplasma
EBV injections

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37
Q

Which groups of women are at higher risk of having a baby with a NTD

A

BMI over 30
Previous child with NTD
FHX
Taking anti-epileptics
Diabetes
Coeliacs
Thalessemia

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38
Q

What does FBC look like in normocytic anaemia

A

Decreased hb
Normal MCV
Normal or increased ferritin
Increased bilirubin
Check reticulocyte count

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39
Q

What can cause G6P deficiency

A

X linked condition - thus affects males more

Anti- malarials
Sulfa drugs ( sulfonamides, sulphasalazine and sulfonylureas)

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40
Q

Causes of macrocytic anaemia

A

Megaloblastic - b12 defieicny, folate defeciency and secondary to methotrexate + pernicious anaemia

Non-megaloblastic - alcohol, liver disease, hypothyroid, pregnancy, reticulocytosis, myelodysplasia and cytotoxic drugs

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41
Q

What does the FBC picture look like for macrocytic anaemia

A

Decreased HB
Increased MCV
Decreased B12 and folate

On blood film hypersegmented neutrophils

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42
Q

What happens to TIBC in anaemia of chronic disease

A

It is Low. In comparison to in iron deficiency anaemia TIBC is high

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43
Q

Causes of hypo proliferative (reticulocyte count) normocytic anaemia

A

Leukaemia
Aplastic anaemia
Pure red cell aplasia
Other BM failure syndromes

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44
Q

What kind of investigations would you carry out to find the causes of microcytic anemia

A

Faecal occult blood test
Endoscopy
Colonoscopy
TTG-IgA test
Flow cytometry - diagnostic for paroxysmal nocturnal haemoglobinuria
Transvaginal ultrasound - may reveal cause of menorrhagia

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45
Q

What is thalessemia

A

Autosomal recessive condition which leads to insufficient haemoglobin production. Affects production of alpha or beta chains .

Most common in Mediterranean, Middle Eastern and Southeast Asians.

Electrophoresis is diagnostic test

Alpha chains coded for via gene on chromosome 16

Beta chains coded for by gene on chromosome 11

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46
Q

What is an important thing to consider in normocytic anaemia

A

Whether reticulocyte count is hypo or hyperproliferative

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47
Q

What causes a hyperproliferatve normocytic anaemia

A

( high production of of rBCS and reticulocyte in response to increased destruction or loss of RBC)

  • haemolytic anaemia caused by
    Drugs - penicillin, levodopa, cephalosporins
    Infections - CMV, toxoplasmosis, leishmania, malaria
    Transfusion reactions
    Burns
    Microangiopathic haemolytic anaemias - HUS, TTP + DIC
48
Q

What kind of anaemia does SCD cause

A

Normocytic hyperprolierative anaemia

49
Q

Etiology of SCD

A

Autosomal recessive condition in which an amino acid substitution leads to production of HbS which in deoxygenated states polymerises causing the characteristic sickle shape and is very rigid.

Causes vaso-occlusive crises and haemolysis. Can also get aplastic crisis where there is a sudden reduction in production of RBC, reticulocyte, WBC and platelets.
Acute chest syndrome - pain, dyspnoea, low sats, infiltrates on CXR
Sequestration crisis - pooling of blood in the spleen and lungs

Diagnosed by electrophoresis

50
Q

How to treat SCD crisis

A

Exchange transfusion??

For recurrent crises patient should be started on hydroxycarbamide

Acute chest syndrome = give antibiotics, oxygen and analgesia

Acute painful crises = IV morphine, fluids and oxygen

51
Q

What test checks for autoimmune haemolytic anaemias

A

Coombs test/ antiglobulin test

Direct test = detects antibodies stuck to surface of RBC

Indirect = detects free floating antibodies in blood

52
Q

What are Howell jolly bodies

A

Red cells which still have nuclear fragments

Often seen in megaloblastic anaemias, hyposplenism and SCD

53
Q

What can cause macrocytic megaloblstic anaemia

A

B12 or B9 deficiency

Malnutrition
Alcohol abuse
Vegan diets
Low protein diets
Pregnancy
Gastric surgery
Anti-folate drugs
Anti-epileptics
Anti-convulsants
Oral contraceptives
Metformin

54
Q

Causes of macrocytic normoblastic anaemia

A

Alcohol abuse
Liver disease
Congenital bone marrow failure syndromes
Myelodysplastic syndrome
Hypothyroid
Pregnancy

55
Q

What is Myelodysplastic syndrome

A

Neoplasm of the bone marrow which affects the stem cells that give rise to the various cell lines. Leads to pancytopenia, anaemia, thrombocytopenia and leukopenia.

Can be idiopathic or secondary to insults to the BM through chemotherapy (alkylating agents*), radiation or exposure to benzene

56
Q

What is hereditary haemorrhagic telangiectasia

A

A type of bleeding disorder:
Fragile dilated capillaries develop on the skin of the lips, nose and fingers which rupture easily
Epistaxis occurs more frequently in these patients

57
Q

What is ehlers Danos syndrome

A

Defect in collagen which makes the blood vessels more weaker and elastic which means the person is at higher risk of:

Easily bruising
Aortic regurgitation
Aortic dissection
Subarachnoid haemorrhage
Mitral valve prolapse

58
Q

What is pseudoxanthoma elasticum

A

When elastic fibres of blood vessels become mineralised due to calcium deposits

59
Q

Examples of platelets disorders:

A

Decreased marrow production (aplastic anaemia or suppression due to cytotoxic drugs or RT)

Bernard soulier disease - platelets are very large and lack protein on surface which allows aggregation to occur

Glanzmanns thromboasthenia - low levels of glycoprotein IIb/IIIa which acts as a receptor for fibrinogen. This interaction normally allows aggregation to occur

thrombotic thrombocytopenic purpura - clotting occurs in small vessels in absence of vascular
injury causing microthrombi to form. Platelets are used up.

Excessive destruction of platelets in immune/idiopathic thrombocytopenic purpura, heparin. SLE + CLL, DIC and HUS

60
Q

What is von wille brands disease

A

Deficiency in Von wille brand factor which is required for platelets to adhere to the endothelium

Also acts as a carrier for factor VIII

61
Q

What is haemophilia A

A

Factor 8 deficiency

X linked recessive condition. Mainly in males but offspring sons will not be affected and daughters will be carriers

May lead to haemarthorosis (bleeding into joints) or haematomas into muscles leading to nerve palsies or compartment syndrome

62
Q

What is haemophilia C

A

Deficiency in factor 11

63
Q

1 unit of RBC is transfused in a non emergency situation over how long

A

90- 120 mins

Those with hf - 3 hours

64
Q

1 unit of RBC increases. HB by

A

10-15g/L

65
Q

1 unit of platelets increases count by

A

20

Indicated when levels are below 30. (Normal is >100 to 400)

66
Q

When is the use of fresh frozen plasma indicated

A

Correct clotting defects (eg DIC)

67
Q

When is cryoprecipitate used

A

Replaces fibrinogen and factor 8 in massive haemorrhages

68
Q

How do acute haemolytic reactions present after transfusion

A

Fevers
Rigours
Hypotension
Tachycardia
Rashes
Pruritus
Red urine
Bleeding
Jaundice
Dyspnoea
Decreased o2 sats

69
Q

How do acute haemolytic reactions present after transfusion

A

Fevers
Rigours
Hypotension
Tachycardia
Rashes
Pruritus
Red urine
Bleeding
Jaundice
Dyspnoea
Decreased o2 sats

70
Q

Examples of delayed reactions that occur after transfusion

A

Infections
Iron overload
Graft vs host disease (donors T cells attack the hosts healthy cells)
Post transfusion purpura

71
Q

What is Haptoglobin

A

Protein produced by the liver which binds to free Hb released from RBC during lysis. It forms a complex which is processed by the liver and removed from the body.

In haemolytic situations levels of haptoglobin become depleted as more is bound to free Hb

72
Q

What cells do myeloid progenitor cells give rise to

A

1) mast cells

2) megakaryocyte —> thrombocyte

3) erythrocytes

4) granulocyte —> basophils, neutrophils and eosinophils

5) monocyte —> macrophage + dendritic cell

73
Q

What cells do lymphoid progenitor cells give rise to

A

1) B cell —> plasma B cell

2) T cell

3) NK cell

4) dendritic cell

74
Q

What is the most common blood cancer in children

A

Acute lymphoid leukaemia

75
Q

What is haemochromatosis

A

Condition in which iron overload occurs.

Most common is hereditary condition which is inherited in an autosomal recessive fashion. There is increased iron absorption which leads to depositions in liver, pancreas, heart and skin leading to liver disease, heart failure, diabetes and skin discolouration

Secondary might be caused by transfusions required in the following disorders: thalessemia, Sickle cell and hereditary spherocytosis

76
Q

What causes anaemia of chronic disease and how is it treated

A

Presents as a normocytic normochromic anaemia

Thought to be related to levels of inflammation affecting levels of EPO

Ferritin levels are high but iron + transferrin is low

Treated with EPO stimulating agent. Can’t be treated with iron as wont be incorporated (+ stimulate erythropoiesis)

77
Q

What common infection can result in haemolytic anaemia as a complication

A

Pneumococcal pneumonia

78
Q

Conditions causing relative polycethaemia

A

Dehydration
Smoking
Hypertension ? Don’t know why

79
Q

What are secondary causes of polycythemia

A

Increased EPO production in renal cell carcinoma
Paraneoplastic syndromes
Chronic hypoxia in COPD and high altitude

80
Q

What are secondary causes of thrombocythemia

A

Bleeding
Inflammation
Infection
Malignancy
Splenectomy

81
Q

Indications of BM aspiration + trephine biopsy

A

Pancytopenia

Lymphoma

Leukaemia

Myeloma

82
Q

Why are levels of LDH increased in anemia and haemolysis

A

Enzyme found within RBC
So when rbc are destroyed prematurely in megaloblastic anaemias and during haemolysis enzyme is released
In ineffective erythrpoeisis there might be hypoxia which might lead to higher levels of this enzyme which is part of anaerobic pathway of respiration

83
Q

Indication of hydroxocobalamin injections

A

Pernicious anaemia B12 deficiency

84
Q

Giving folate in b12 deficiency might lead to

A

Subacute combined degeneration of the cord

85
Q

What is ALL

A

Acute lymphoblastic leukaemia

A form of leukaemia in which the bone marrow produces lots of immature lymphocytes ( B + T cells)

Symptoms include

Fatigue, SOB, fever, easy bruising, bone pain, swollen lymph nodes and weight loss and lack of appetite

Signs:
Lymphadenopathy, hepatosplenomegaly, nuchal rigidity

Risk factors:
- chromosomal aberrations like downs
- previous chemo or RT
- high levels of radiation
- genetic

Occurs in children most commonly, peak in mid 30s and 80s

86
Q

Treatment of ALL

A
  • induction chemo (to get rid of immature blasts)
  • adjunct meds to prevent toxicity to other organs
  • rituximab
  • prophylactic antimicrobials
    -haematopietic growth factor
87
Q

Who does CLL affect

A

Most common leukaemia
Affects males more than females
Median age of diagnosis is 70

88
Q

What are the symptoms of CLL and pathophysiology

A

Affects mature lymphocytes which are functionally abnormal (mostly B cells) - accumulate in the BM preventing normal BM function

Causes:
- chromosomal abnormalities and mutations in proteins involving tyrosine kinase pathway

Risk factors:
- age
- FHX
- agent orange exposure from Vietnam war

B cells might produce abnormal antibodies that might lead to autoimmune haemolytic anaemia, ITP

Treated with chemoimmunotherapy (tyrosine kinase inhibitors)

89
Q

What organs can leukaemias infiltrate

A

Bone marrow —> bone pain

Thymus —> palpable mass and airway compression

Liver + spleen —> hepatosplenomegaly

Lymph nodes —> lymphadenopathy

Meningeal infiltration —> headaches, vomiting, nerve palsies + nuchal rigidity

90
Q

What labs would you request for investigation of leukaemia

A

Blood count
Blood smear/film
BM smear
Immunophenotyping

91
Q

What is AML:

A

Affects myeloid lineage with rapid production of immature blasts that are unable to mature into neutrophils, RBC, platelets. This leads to BM failure

Risk factors:
Age 60 peak
RT or chemo
Downs
Myeloproliferative disorders such as PRV or thromobocythemia
Radiation or benzene exposure

On smear presence of Auer rods

Treated with chemo
Retinoic acid treatment for promyelocytic anaemia

92
Q

What is richter syndrome

A

Transformation of CLL or small lymphocytic lymphoma to high grade diffuse large B cell lymphoma

93
Q

Which leukaemia may progress to aggressive lymphoma (diffuse large B cell lymphoma)

A

CLL

94
Q

What is CML

A

Form of leukaemia in which there is increased myeloid cells. This is caused by a genetic abnormality - formation of the Philadelphia chromosome (9+22 translocation) which results in BCR-ABL gene which produces increases in protein called tyrosine kinase —> uncontrolled growth

Has stages:
1) chronic phase
2) accelerated ophase
3) blast phase (behaves like an acute leukaemia)

Risk factors:
-age
-radiation and benzene exposure

Treatment:
- tyrosine kinase inhibitors like imatinib

95
Q

What is myeloma

A

Terminally differentiated neoplastic plasma cells which produce antibodies uncontrollably. Produces lots of fragments + light chains (paraproteins) IGA and IGG

Associated with osteolytic bone disease, renal failure and anaemia. Leads to amyloidosis and hyper viscosity syndrome (heart has to work harder)

Symptoms: CRABBI
Hypercalcemia
Renal failure
Anaemia
Bone pain/lesions
Bleeding
Infections

Investigations:
-electrophoresis
- bence jones proteins in urine
MRI - for bony lesions

Treatment:
Chemo, RT, immunotherapy + transplants

96
Q

What is first line therapy for hypercalcemia

A

IV 0.9% saline

97
Q

What is tumour lysis syndrome

A

A complication of chemo in which cancer cells die and release toxins which the body is not able to get rid of as quickly.

Hyperuricemia, hyperphopshatemia, hyperkalemia, uraemia, hypocalcemia and acute renal failure.

IV rasburicase used to treat this.
Allopurinol used as prophylaxis

98
Q

What is lymphoma

A

Malignancy of the lymphatic tissues and lymph nodes affecting lymphocytes. Usually starts off in a node or tissue (spleen, thymus + other organs) and may spread to BM + other parts of body.

Hodgkins - characterised by presence of reed sternberg cells (giant cells with more than 1 nucleus arranged in a mirror fashion (looks like owl eyes) )
Occurs in early adulthood

Non Hodgkins - classified at B or T type (most common type 90%) with B cell more common. There are a lot of types within these two categories
Affects older people >60

99
Q

What staging system is used for Hodgkin lymphoma

A

Ann arbor

Looks at symmetry of lymph node involvement

100
Q

Types of Hodgkin lymphoma

A

Nodular sclerosing - most common. Occurs more in young women affecting lymph nodes of central chest - good prognosis

Mixed cellularity - many different WBC types - good prognosis

Lymphocyte rich - m>w. Has many normal lymphocytes along side reed sternberg cells. Best prognosis

Lymphocyte depleted - occurs in those with HIV/AIDS. Replacement of normal cells with R/S cells - worst prognosis

101
Q

Risk factors for Hodgkin’s lymphoma

A

Older age
Males
Family history
Infections: HIV, HEP C, EBV, HHV-8, h.pylori, C.jejuni.
Autoimmune disease: hashimotos,coeliac, Sjögren’s syndrome, RA + SLE

102
Q

Investigations for lymphoma

A

FBC
Imaging - CT + PET
Lymph node biopsy

103
Q

Investigations for lymphoma

A

FBC
Imaging - CT

104
Q

Treatment regime for Hodgkins AVBD: or BEACOPP

A

Doxorubicin (Adriamycin)
Vinblastine
Bleomycin
Dacarbazine

Bleomycin
Etoposide
Doxorubicin
Cycklophasmide
Vincristine/oncovin
Procarbazine
Prednisolone

105
Q

Examples of B cell non Hodgkins lymphomas

A

Burkitts lymphoma (associated with EBV + malaria) aggressive

Diffuse large B cell lymphoma (most common but aggressive)

Mantle cell lymphoma (aggressive)

Follicular lymphoma (non-aggressive)

CLL

Marginal zone lymphoma

106
Q

Examples of T cell non Hodgkin’s lymphoma

A

Adult T cell lymphoma

Cutaneous T cell lymphomas (formation of itchy plaques)

107
Q

Treatment of non Hodgkin’s lymphoma RCHOP

A

Rituximab
Cyclophosphamide
Doxorubicin
Vincristine/oncovin
Prednisolone

108
Q

Examples of myeloproliferative disorders

A

PRV (excessive RBC caused by JAK-2 mutation)
Essential thrombocythemia (excessive platelets which can block vessels and flow. Or can cause excessive bleeding as all might be used in clotting)
ET might progress to PRV, myelofibrosis or AML

109
Q

Signs and symptoms of PRV

A

PE
DVT
Splenomegaly
Excessive bleeding
Kidney stones and gout (high RBC turnover causes high urate levels)
Stomach ulcers (high RBC levels leads to immune response and release of histamine which acts on parietal cells to secret more acid)

110
Q

Examples of JAK inhibitor

A

Ruxolitinib

111
Q

Treatments for PRV

A

Venesection
Low dose aspirin
Allopurolol
Ruxolitinib
BM transplant

112
Q

Treatment for ET

A

Aspirin
Interferon alpha (stops platelets dividing)
Hydroxyurea 9reduces platelet count)
Ruxolitinib
Chemo
Plateletpheresis (machine removes platelets

113
Q

What is myelofibrosis

A

Most aggressive MP disorder: caused JAK-2 =, CALR and MPL mutation.

BM produces abnormal stem cells that become inflamed and make scar tissue. This stops production of other blood cells. RBC low, WBC + P may increase at first but will suddenly drop

Anaemia, fevers, night sweats, weight loss, splenomgealy (massive) and easy bruising

114
Q

Treatments for myelofibrosis

A

JAK inhibitor
Blood transfusions
Chemo
Splenectomy if speeen too damaged
Androgens can boost RBC production

115
Q

What is myelodysplasia

A

Blood cancer where BM stem cells don’t mature and die leading to pancytopenia. Can progress to AML

Causes include:
- fanconi anaemia
- diamond black fan anaemia
- previous chemo = RT
- exposure to heavy metals

116
Q

Treatment for myelodysplasia

A

Blood transfusions + platelet
Antibiotics
Chemo
Stem cell transplants

117
Q

What is fanconi anaemia

A

Rare autosomal disorder in which there is impaired DNA repair machinery which leads to genetic damage —> pancytopenia

Block 34 Metabolic Flashcards (5 decks)

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