Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HAEMOTOLOGY > MedEd Lecture 2 > Flashcards

MedEd Lecture 2 Flashcards

1
Q

Anaemia values in men and women

A

Men = < 130g/ml
Women = <120g/ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Three general mechanisms behind anaemia

A
  1. Blood loss
  2. Decreased RBC production
  3. Increased RBC destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of microcytic anaemia

A

Iron deficiency, thalassaemia, sideroblastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Most common cause of iron deficiency anaemia

A

blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Key features of iron deficiency anaemia on film and blood test

A

Pencil cells on peripheral blood smear

Decreased iron, ferritin

Increased transferrin and total iron binding capacity

Reactive thrombocytosis - iron normally inhibits thrombopoiesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Iron study results in iron deficiency anaemia and why

A

Low iron and ferritin - due to lower storage of iron

Increased transferrin - to try and compensate and increase iron transport

Increased total-iron binding capacity - because you transferrin is better at keeping a hold of iron when you really need it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Key features of thalassaemia on blood smear

A
  • basophilic stippling = aggregation of basophilic granules dispersed through the cytoplasm of erythrocytes
  • target cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Iron study in thalassaemia

A

normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is sideroblastic anaemia?

A

Basically you have enough iron but you can’t incorporate it into the haemoglobin

You get iron build up forming ringed siderblasts (erythroid precursors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens to the mitrochondira in siderblastic anaemia?

A

iron gets stuck in them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes of siderblastic anaemia

A

Congenital

Acquired - excessive alcohol, lead poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Key features of siderblastic anaemia

A
  • basophilic stippling
  • iron studies: raised iron, ferritin, low transferrin, low total-iron binding capacity
  • bone marrow: ringed sideroblasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of macrocytic anaemia

A

Megaloblastic: B12 deficiency, folate deficiency

Non-megaloblastic: alcohol, hypothyroidism, pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does alcohol cause macrocytic anaemia?

A
  • deposition of cholesterol into erythrocyte membrane increases the size of the cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does hypothyroidism cause a macrocytic anaemia?

A

T3 helps with EPO production which are needed for RBC production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How to differentiate B12 deficiency and folate deficiency anaemia

A
  • Duration - folate = months, B12 = years
  • Clininal - B12 = neurological changes
  • Methylmalonic acid is raised in B12 deficiency
    Schilling test - positive in B12 secondary to pernicious anaemia
  • Drug Hx - phenytoin inhibits folate absorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Megaloblastic vs non-megaloblastic

A

Megaloblastic has hypersegmented neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes of normocytic anaemia

A
  • Haemolytic: inherited or acquired (immune-medicated or non-immune mediated)
  • Non-haemolytic: anaemia of chronic disease, failure of erythropoiesis
19
Q

What is anaemia of chronic disease and what are the iron studies?

A

Secondary to infection, inflammation, malignancy

  • immune system gets activated by auto-antigens, tumour antigens etc and that increases cytokine production, which increases hepcidin
  • Hepcidin stops the absorption of iron in the intestine
  • So iron storage goes up so increased ferritin and iron, decreased transferrin and TIBC
20
Q

Causes of inherited haemolytic anaemia

A
  1. Membrane affected = Hereditary Spherocytosis
  2. Cytoplasm affected: G6PD deficiency
  3. Haemoglobin affected: Sickle cell
21
Q

Causes of acquired haemolytic anaemia

A
  1. Immune: autoimmune warm vs cold, alloimmune: ABO or rhesus
  2. Non-immune: microangiopathic vs macroangiopathic, infection,
22
Q

Inheritance of hereditary spherocytosis

A

autosomal dominant

23
Q

What is hereditary spherocytosis?

A
  • defect in vertical interaction (proteins) of the red cell membrane
24
Q

Key features of herediatry spherocytosis in terms of tests

A
  • peripheral blood smear = spherocytes, polychromasia
  • positive osmotic fragility test (more fragile)
  • positive eosin-5-maleimide (basically a specific substance isn’t taken up as much cos the membrane is shit)
25
Q

Management of hereditary spherocytosis

A
  • folate
  • splenectomy
26
Q

Inheritance of G6PD

A

X-linked recessive (so men affected more)

27
Q

In simple terms what is G6PD deficiency

A
  • the enzyme is needed to help RBCs work correctly and protect them from oxidative stress
28
Q

Key features of G6PD

A
  • episodes of acute haemolysis following exposure to oxidative stress (fava beans, Abx, malaria drugs)
  • Heinz Bodies (denatured Hb in RBC), Bite Cells (half denatured RBCs by phagocyte)
  • Intravascular haemolysis: raised unconjugated bilirubin, decreased haptoglobin (gets used up cleaning up Hb), haemoglobinuria
29
Q

Mx of G6PD

A

avoid trigger

30
Q

Difference between warm and cold autoimmune haemolytic anaemia

A

Warm (above 37) = IgG, associated with CLL, extravascular haemolysis)

Cold (28-31) = IgM, associated with mycoplasma, EBV, Hep C, intravascular haemolysis

31
Q

How is autoimmune haemolytic anaemia managed?

A

treat underlying cause, steroids, rituximab

32
Q

Key test form autoimmune haemolytic anaemia

A

Direct Coombs test (dat scan)

  • anti-human globulin given with human RBC
  • see if it attached to the antigen
33
Q

MAHA mechanism

A
  • non-immune mediated haemolytic anaemia
  1. Damage to the endothelial cells within the vasculature
  2. Fibrin deposition and platelet aggregation
  3. Fragmentation of RBCs moving through (schistocytes)
34
Q

Key features of MAHA

A
  • schistocytes, thrombocytosis
  • background of HUS, TTP, DIC
  • normal APTT, PT, fibrinogen
35
Q

most common cause of HUS

A

E.coli O157:H7 - shiga-like toxin

36
Q

Typical presentation of HUS

A

Kid who had diarrhoea but now has renal failure, low platelets, MAHA

37
Q

Key features of HUS

A
  • symptoms after diarrhoea illness
  • don’t give Abx
  • MAHA, thrombocytopenia, renal failure
  • features of MAHA on smear
38
Q

What is TTP

A

Thrombotic Thrombocytopenic Purpura

  • deficiency of ADAMTS13 which results in decreased breakdown of multimers of vWF so you get big clots
  • inherited or acquired
39
Q

Key features of TTP

A
  • MAHA, thrombocytopenia, acute renal failure, neurological symptoms, fever
  • high mortality rate
40
Q

Mechanism of DIC

A
  • activation of both coagulation and fibrinolysis triggered by:
  • sepsis (most common)
  • trauma
  • obstetric complication
  • malignancy
41
Q

Coagulation screen in DIC

A

decreased platelets, fibrinogen
raised PT, APTT, d-dimer

42
Q

Causes of MAHA

A

HUS, TTP, DIC

43
Q
A

HAEMOTOLOGY (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions