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YEAR 2 S2 PATHOLOGY > Blood II > Flashcards

Blood II Flashcards

1
Q

describe anaemia of chronic diseases

A
  • one of the most common anaemias
  • associated w/ RED RBC prolif, impaired Fe UTILISATION
  • associated w/ CHRONIC MICROBIAL INF (eg osteomyelitis), CHRONIC IMMUNE DISORDERS (eg rheumatoid arthiritis), NEOPLASM (Hodgkin’s lymphoma, lung carcinoma)
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2
Q

what is the pathogenesis of anaemia of chronic diseases

A

CYTOKINE DRIVEN INHIBITION OF RBC PRODUCTION

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3
Q

what are the lab features of anaemia of chronic diseases

A
  • LOW serum iron
  • LOW iron binding capacity
  • INC storage iron in marrow macrophages
  • RBC: normochromic/normocytic
    microcytic and hypochromic (as in iron deficiency anaemia)
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4
Q

what are the clinical features of anaemia of chronic diseases

A
  • anaemia not severe

- the most dominant symptoms are those of underlying diseases

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5
Q

what is the treatment for anaemia of chronic diseases

A
  • treat UNDERLYING CONDITION

- patients may benefit from from EPO

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6
Q

what is aplastic anaemia

A

Defined as pancytopenia (anaemia, neutropenia, thrombocytopenia) with hypocellularity of bone marrow

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7
Q

how common is aplastic anaemia

A

Uncommon but serious condition

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8
Q

what is the cuase of aplastic anaemia

A
  • May be inherited; more commonly acquired
  • Probably results from failure or suppression of pluripotent stem cells
  • Very occasionally, defect of the erythroid series only - “pure red cell aplasia”

MAJOR CAUSES:

1) Idiopathic
- Primary stem cell defect
- Immune mediated
2) Chemical agents
- Dose related (alkylating agents, benzene)
- Idiosyncratic (chloramphenicol)
3) Physical agents
- Whole body irradiation
4) Viral infections
- Hepatitis (unknown virus)
- Cytomegalovirus infection
5) Miscellaneous
- Infrequently, many other drugs and chemicals

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9
Q

what are the clinical features /symptoms and physical findings of aplastic anaemia

A

Symptoms - results of the deficiency of:

  • Red blood cells (anaemia)
  • White blood cells (susceptibility to infection)
  • Platelets (bleeding)

Physical findings:

  • Bruising, bleeding gums and epistaxis
  • Mouth infection common
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10
Q

what investigations can be done for aplastic anaemia

A

1) Blood count
- Pancytopenia
- Low or absent reticulocytes
2) Bone marrow examination
- A hypocellular marrow withincreased fat spaces

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11
Q

how can we have a differential diagnosis of aplastic anaemia compared to other causes of pancytopenia

A

Bone marrow biopsy :bone marrow cellularity

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12
Q

what is the treatment for aplastic anaemia

A
  • Withdrawal of offending agent
  • Supportive care (infection control)
  • Specific treatment (bone marrow transplantation; immunosuppressive therapy)
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13
Q

describe haemoglobin abnormalities

A
  • Mostly caused by single point mutation
  • Abnormal globin chain structure
  • Imbalanced globin chain production
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14
Q

describe sickle cell

A
  • disease of abnormal ß globin chains
  • Common in people of African origin
  • cause: : homozygous inheritanceof a gene coding for a haemoglobin variant (HbS) single base mutation (A –> T) causes (Glutamine –> Valine)
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15
Q

what is the pathogenesis of sickle cell

A
  • HbS crystalline at low O2 tension

- causes Shortened RBC survival and Impaired passage through microcirculation

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16
Q

what are the clinical features of sickle cell

A

characterized by tissue infarction and chronic haemolysi:

  • Vaso-occlusive crises (acute pain in hands/feet; severe pain in other bones)
  • Anaemia (chronic haemolysis or acute fall in Hb)
  • precipitated by other factors (infection, dehydration, cold, acidosis, hypoxia)

Heterozygous state (sickle cell trait): no symptoms

17
Q

what investigationc can be done for sickle cell

management

A

Investigations:
- Blood count: Hb range 6-8 g/dl, reticulocytes 10-20%−Blood film: sickled RBC

MANAGEMENT:
−Asymptomatic: no treatment
−Avoid precipitating factors
−Acute painful attacks: supportive therapy
−Severe haemolysis: folic acid
−Infection: prophylaxis (antibiotics, vaccine)−Anaemia as indicated (transfusion, hydroxycarbamide)

18
Q

what are thalassaemias

A

cause: : abnormalities of globin chain (a or b)synthesi

19
Q

what is the pathogenesis of thalassaemias

A

imbalanced’globinchain production –> globin chains in RBC –> ineffective erythropoiesis& haemolysis

20
Q

what are the types of thalassaemias

A
  • b-thalassaemia major (b chain production↓):
    Severe anaemia from infancy, Splenomegaly,Marrow expansion
  • b-thalassaemia minor:
    Clinically mild
  • a-thalassaemia (a chain production↓):
    Range from severe anaemia to clinically insignificant disease
21
Q

what are the laboratory tests for thalassaemias

A

Blood count and film:
- Hypochromic/microcytic anaemia
- Reticulocytes ↑
−Nucleated red cell

Diagnosis by haemoglobin electrophoresis
- INC in Hb F and DEC in Hb A

22
Q

what is an example of red cell enzyme deficiency

A

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

23
Q

(G6PD) deficiency causes what

A

haemolytic anaemia

24
Q

what is (G6PD) deficiency

A
  • G6PD deficiency is the chief RBC enzyme defect
  • Affecting 100million people, mainly male
  • A common heterogeneous X-linked trait, predominantly in Africa, Mediterranean and Middle East
25
Q

describe G6PD

A
  • G6PD is a vital enzyme in hexose monophosphate shunt, which maintains glutathione in the reduced state (GSH)
  • GSH protect against oxidant injury in RBC
  • G6PD deficiency reduces the ability of RBC to protect against oxidative injuries
  • This leads to haemolysis
26
Q

what is the genetics behind G6PD deficiency

A
  • Over 400 G6PD variants; mostly single AA substitutions
  • The most common types have normal activity:
    • Type B+, almost all Caucasians and 70% black Africans
    • Type A+, about 20% of black Africans
  • Two common variants with reduced activity :
    • African (A-) type, mild deficiency and more marked in older cells. Haemolysis is self-limiting
    • Mediterranean type, both young and old red cells have very low enzyme activity; serious clinical consequenc
27
Q

what are the clinical manifesations of G6PD deficiency

A
  • Most are asymptomatic, but may get oxidative crisis when precipitate
  • Neonatal jaundice
  • Chronic haemolytic anaemia
  • Acute haemolysis, precipitated by
    • Ingestion of broad beans
    • Administration of oxidising drugs (quinine, sulphonamides)
    • Infection and acute illness
28
Q

what investigations can be done for G6PD

A
  • Blood count normal between attacks
  • During an attack:
    • Blood film – bite cells, blister cells
  • Haemolysis (serum bilirubin↑)
  • Measurement of G6PD level
29
Q

what is the treatment for G6PD deficiency

A
  • Avoid precipitating factors
  • Transfusion if necessary
  • Treat the underlying infection

YEAR 2 S2 PATHOLOGY (22 decks)

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