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Phase 3 > Haematology > Flashcards

Haematology Flashcards

1
Q

What is Haemophilia A? What are the sub-categories?

A

Factor VIII Deficiency

Mild - surgical bleeding

Moderate - minor trauma bleeding

Severe: - spontaneous bleeding

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2
Q

How is haemophilia A transmitted?

A

X-linked

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3
Q

How does Von Williebrand disease present?

How is it transferred?

A

Mucosal Surface bleeding

Heavy periods

Woulds bleed heavily

*autosomal dominant

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4
Q

What other factor will be low in Von Williebrand disease, and why?

A

Factor VIII - it prolongs the half life of the factor.

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5
Q

Name two severe platelet disorders and the underlying pathology:

How are these transferred?

A

Glansmanns Thrombasthemia:
- lack GP IIb/ IIIa

Bernard Soulier Syndrome:
- lack GPIb/ V/ IX

*autosomal recessive

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6
Q

In Lupus Anti-coagulant disease, what would you expect to see on tests, and how does this correlate to in the body?

A

Increased APTT time

Paradoxically increased thrombus formation in the body.

DRVVT pre-longed. fixed with excess phosoplipids.

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7
Q

What is the pathology of Lupus causing increased APTT?

A

Antiphospholipid antibodies

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8
Q

How much Fe2+ is in the R.E.S?

A

200-500mg.

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9
Q

What disease may skew the serum ferritin results and why?

A

Inflammatory disease such as RA.

Because Serum ferritin is a inflammatory protein.

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10
Q

What “other” symptoms may be present in iron deficient anemia?

A

Koilonychia

Atrophic Glossitis

Angular Stomatitis

Oesophageal web

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11
Q

If 200mg of ferrous sulphate is given, what is the elemental amount of iron absorbed?

A

60mg - 30%

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12
Q

Why do people develop anaemia in pro-longed inflamamtion/ disease?

A

prolonged inflammation increases Hepcidin.
this reduces absorption and release from R.E.S

ILs released from inflammation may also shut down marrow activity.

EPO is also supressed

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13
Q

In anaemia of chronic disease, what different lab findings would you have to iron deficient anaemia?

A

ESR will be raised

Ferritin levels will be raised

Total iron levels will be reduced

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14
Q

What receptors do B12 bind with in the gut and where are these predominantly found?

A

Cubulin

in the ileum.

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15
Q

How is B12 transported in the blood?

A

Transcobalamin

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16
Q

What are some symptoms of B12 deficiency?

A

Anaemic symptoms

Mild jaundice - ineffective RBC production

Neurological disturbances - especially the posterior pyramidal tracts

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17
Q

In megoblastic anaemia, what do the blood cells look like?

A

Macrocyctic

Very Red

HIgh MVC

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18
Q

What chromosome is globin A made on?

A

Chromosome 16

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19
Q

What chromsome is Globin B, Gamma and delta made on?

A

Chromosome 11

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20
Q

How many genes code for Alpha globin?

A

4 genes

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21
Q

If there is 1 gene missing from Alpha globin, what is the disease state?

A

Alpha thalassemia trait - mild microcytosis

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22
Q

If the person has 2 gene missing for alpha globin, what is the disease state?

A

Alpha Thalasemia minor

  • microcytosis
  • Low MVC
  • increased red count
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23
Q

If there is 3 genes missing from alpha globin, what is disease state?

A

Hb Disease

  • leads to haemolysis in spleen due to bizzare shape
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24
Q

what is it called when there is 4 genes missing from alpha genes?

A

Barts Hb.

incompatible with life.

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25
Q

What is beta thalassaemia major?

A

both genes for beta globin missing.

Symptoms appear after fetal globin is gone.

Extra-medullary areas try and produce RBCs - especially skull

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26
Q

What is another complication of Beta thalassaemia?

A

Haemochromotosis - hepcidin is reduced in order to try and increased Fe2+ levels.

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27
Q

What is the genetic mutation in sickle cell disease?

A

Non conservative single base pair change to the Beta globulin chain.
- thus affects children >6 months

glutamie to valine.

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28
Q

What are some serious complication of sickle cell disease?

A

Vaso-occlusion

  • tissue hypoxia
  • stroke
  • infarction
29
Q

What disease causing changes in the membrane leading to sphere like appearance and what is the protein defective?

A

Hereditary spherocytosis.

Spectrin

30
Q

What is the outcome of Hereditary spherocytosis?

A

haemolysis in the spleen. RBCs unable to fit through mesh.

31
Q

What disease leads to RBCs being unable to cope with oxidative tress?

A

Glucose - 6 - Phosphate DEhydrogenase Deficiency.

lack of Glutathione

32
Q

What immunoglobulin is indicating in warm type haemolytic anaemia?

A

IgG

33
Q

What immunoglobulin is indicated in cold type haemolytic anemia?

A

IgM

34
Q

What is the initial treatment for warm haemolytic anaemia?

A

Steroids
blood transfusion is patient is gravely ill and can’t wait for steroids to work

Splenectomy

35
Q

What is the name of Glandular fever? and what virus causes it?

A

Infectious mononucleosis

Epstein Barr virus

36
Q

What two important LFT may be elevated in haemolysis of RBCs?

A

Bilirubin

Lactate dehydrogenase

37
Q

In Immunothrombocytopenia would you expect to see an enlarged spleen?

A

No - the platelets are too small

38
Q

Can amoxicillin be given for Glandular fever?

A

No. causes bad rash.

if antibiotics are needed then only Penicillin B

39
Q

What factors are used up in Haemolytic Uraemic Syndrome?

A

Platelets

40
Q

If the spleen is removed, what kind of RBCs may be seen that still contain their DNA?

A

Howell Jolly Body cells

41
Q

Which disease is much more severe when the spleen is removed?

A

Malaria

42
Q

If a person has sphere shaped RBCs and a coombes test is performed and it comes back negative, what does this mean?

A

means they don’t have auto immune disease and that their sphere shaped cells is due to autosomal dominant sphereocytosis

43
Q

What blood disease is associated with other autoimmune disease, and will cause CNS dysfunction?

A

Pernicious anemia

44
Q

What is a paediatric vasculitis that causes strange rash formation?

A

Henoch Scholien

45
Q

If there is a purpuric rash, what type of meningitis can this be a symptom off?

A

meningococcal sepsis

46
Q

Thombophilia Inherited affects what? and how is it inherited?

A

Anti-thrombin
Protein C
Protein S

Autosomal dominant

47
Q

How is Beta thalaseamia inherited?

A

Autosomal recessive

48
Q

Who is most likely to inherit Spherocytosis?

A

Northern Europeans - autosomal dominant

49
Q

How is G-6-PD inherited and who is most likely to get it?

A

X-linked.

Africans.

50
Q

What activates protein C and protein S, and what does it need to bind with to be activated?

A

thrombo-modulin.

Needs to be bound to IIa

51
Q

What infections are of particular concern when a person has their spleen removed and how is this managed?

A

Nisseria Meningitis

Haemophilus Influenza

strep pneumonia

Treated with prophylactic amoxicillin for life and vaccinations

52
Q

What disease may Heinz bodies and bite cells be seen?

A

Glucose - 6 - dehydrogenase deficiency

53
Q

What is something you must always ask a Sickle Cell patient?

A

Have they got chest pain, or cough.

thinking about acute chest syndrome

54
Q

What kind of haemolysis is sickle cell disease?

A

Intravascular

55
Q

Where is an aspirate of bone marrow taken from?

A

Iliac Crest

56
Q

Whats it called when CO2 dissolves into the RBC?

A

Chloride Shift

57
Q

How do the macrophages of the RES get iron?

A

Break down of old RBCs

58
Q

How much is each mmol of Ferritin inequivalent too of iron stores?

A

1mmol/L = 8mg of Iron

59
Q

What is it called where there is a reduction in the RES Iron stores, but the bone marrow maintains a normocytic anaemia by using what there is?

A

Latent Iron Deficiency
- 20% of females have this

Low ferritin but normalcyctic cells

60
Q

Whats the most common anaemia in hospital patients?

A

Anaemia of chronic disease

61
Q

Generally speaking what does roulex in the RBCs mean?

A

High ESR but can be associated with myeloma

62
Q

What are the key roles of B12?

A

Methylation of homocysteine to methionine

Methylone isomerization of CoA

63
Q

What skin conditions may need increase folate and B12 intake?

A

Psoriasis

64
Q

If you have petechia, what is this suggestive off?

A

Small capillary bursts with platelet disorders

65
Q

How do you treat platelet disorders?

A

Platelets transfusion
- HLA matched

Tranexamic Acid

66
Q

What may someone have if they continually get DVTs?

A

Thrombophilia

Deficiencies:
Antithrombin *most common
Protein C
Protein S

67
Q

Name the types of warm haemolytic anaemia, and the management of this:

A

Primary - idiopathic

Secondary - acquired. SLE, CCL, Non-hodgkin lymphoma

Steroids

Blood transfusion - those that can’t wait for steroids to work

Folic Acid

Splenectomy

  • S. Pneumoniae
  • H. Influ
  • N. Meningitis
68
Q

What your investigations into Anaemia?

A

FBC

Blood Film

Iron

Ferritin

Transferrin/ TIBC

B12

Folate

LFTs
- haemolytic causes

Chest x-ray
- suspicious of cancer

*check for bleeding

Serum electroplates if suspect Bence jones

Comb’s test if suspecting anything

69
Q

What is the relationship between Ferritin and TIBC?

A

Indirect - as one goes up the other will go down.

this is important to establishing between anaemia of chronic disease and iron loss anaemia

Phase 3 (50 decks)

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