Brainscape's Knowledge GenomeTM

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


See full index

Lucy Knox - Year 2.5 > 231 - Anaemia > Flashcards

231 - Anaemia Flashcards

1
Q

What is the role and properties of erythrocytes?

A 
Carries O2 and plays role in pH buffering
- felxible
Strong
Biconcave
Hb filled

120 days lifespan

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

Describe the steps of erythropoeisis

A

1) EPO from peritubular cells in renal cortex stimulates stem cell sin bone marrow -> erythroid precursor
2) Maturation - Iron supplied to erythroid progenitor cells by macrophages, and the nucleus is removed -> erythrocytes

Pronormocytes -> normoblasts -> reticulocytes (released into blood stream)-> anucleate -> erythrocyte (no organelles, high Hb content)

EPO isn’t stored but made in response to tissue hypoxia

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

How do you get anaemia from chronic renal disease?

A

EPO produced in kidneys normally

so in disease - EPO reduced, so less reticulocytes pushed into development -> normocytic anaemia

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

When you have chronic aneamia, what happens to the BM?

A

The chronic hypoxic state causes EPO to be increased, so you get increased erythroblast production and expansion - causes fatty deposition in the BM -> deformities

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

What are haematinics?

A

The key micronutrients that are needed for RBCs

eg. Iron, B12, Folate

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

How is Iron absorbed and used in the body?

A

Absorbed from the GI tract
Attached to transferrin in plasma
Some binds to apoferritin to be stored in liver
Rest goes to BM
Recycled by the reticuloendothelial system

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

What happens if you have iron deficiency in the BM?

A

Increase number of reticulocyte devisions to make Hb conc high enough

  • Microcytic and low Hb - hypo-chromic RBCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a good measure of iron levels in an inflammatory state?

A

STFr - Soluble Transferrin receptor - doesn’t get affected in inflammation

Raised in anaemia / iron deficienct

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

What is the biochemical profile of iron deficiency anaemia?

A

Reduced Serum Iron
Reduced serum ferritin
Increased total Fe binding capacity
Increased STFr

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

How is Vit B12 absorbed?

A

Ingested + binds with Intrinsic factor (produced by parietal cells in stomach)
Absorbed in distal ileum

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

What type of anaemia do you get in Vit B12 or folate deficiency?

A

Macrocytic - slower RBC synthesis, less DNA so less devisions

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

What is Hereditary spherocytosis / Hereditary elliptocytosis?

A

Causes RBCs to be spheres / abnormally large- as autosomal dominant condition causes defect in protein : Spectrin

Causes haemolytic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What 4 proteins are key in RBC membranes to allow them to keep their shape and strenght?

A

Spectrin
Actin
Protein 4.1
Ankyrin

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

Describe metabolism in a RBC

A

With no cell organelles and no mitochondria the fully developed erythrocyte relies on the glycolytic aerobic pathway to gain energy (ATP) for the cell.

Detoxification of waste products (from oxidative substrates) is done via the Hexose monophosphate shunt.

This requires Pyruvate kinase and Glucose-6-phosphate dehydrogenase (G6PD) , both of which can have deficiencies causing anaemic diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What makes up Hb to help it carry O2?

A

4 globin chains (2 alpha 2 beta)
Iron molecule
A molecule called 2,3 – Diphosphoglycerate (2,3-DPG)sits between the  chains and when increased helps to offload more oxygen to the tissues.

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

Describe thalassaemia briefly in terms of aneamia

A

In thalassaemia there is a reduced rate of synthesis of either alpha or beta globin chains.

Within this group of inherited conditions there may be both ineffective erythropoiesis and haemolysis leading a
hypochromic microcytic anaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe Sickle Cell breifly

A

Sickle cell disease there is an inheritance of two abnormal beta-chain genes (HbSS).

The abnormality consists of a point mutation in the beta globin gene. The result is one of Hb insolubility in it’s deoxygenated state and crystallization within the red blood cell causing sickling of the cell and vascular occlusion.

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

What is the shape of the O2 dissociation curve?

A

Sigmoid curve
As O2 is unloaded the B chains pull apart
2-3 DPG enters this space - reduces the affinity to O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What shifts the O2 dissociation curve to the left?

A

Increased pH, low CO2, Low DPG

Causes increased affinity to O2 - easier binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What shifts the O2 dissociation curve the the right?

A

Low pH, High CO2/H+ in the RBC, High DPG

Reduces the affinity to O2 - harder binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What can you measure to investigate heamolysis?

A

Lactic acid dehydrogenase (LDH) - nucleic enzyme released on RBC breakdown

Reticulocyte count - elevated in haemolysis due to feedback telling BM to produce + release more RBCs

Bilibrubin - The phosphrotin in heam broken down into bilirubin, which gets bound to albumin in plasma. If excess unconjugated -> gets conjugated in liver and excreted in faeces (stercobiligin) or urine (urobiligin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What Hb level defines anaemia?

A

For adult males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What compensatory mechanisms are activated in anaemia? What signs do they show?

A

CVS - Increase stoke vol + increasing HR (so feel palpitations)

Skin - vasoconstriction so blood redistributed to key areas - see palor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What clinical signs are seen in anaemia?

A

Pallor of mucous membranes
Peripheral oedema
High flow murmur
Koilonychia (iron deficiency anaemia)
Atrophic glossitis (folate /B12 deficiency)
Angular stomatitis (folate/B12)
Dysphagia: pharyngeal web (iron deficiency)

25
Q

Within the developing world iron deficient anaemia is the single greatest cause of anaemia? T of F?

A

True

26
Q

The respiratory system is the main physiological compensator in an anaemic patient? T of F?

A

False - CVS is

27
Q

Koilonychia, glossitis, angular stomatitis are all general signs of anaemia? T or F?

A

False
Koilonychia - iron deficiency
Angular stomatitis - B12/folate

28
Q

How long do platlets last for/

A

8-10 days

29
Q

What blood cells are from the myeloid projenitor cells?

A

Monocytes
Neutrophils
Eosinophils
Basophils

30
Q

Which blood cells are from the lymphoid progenitor cells?

A

B cells -> plasma cells

T cells

31
Q

What is the common embryological origin of the blood system?

A

Aorta Gonad mesonephros

From yolk sac -> liver -> bone marrow

32
Q

In the foetus where is blood produced?

A

First in yolk sac
Then Liver + small amount in spleen
Then bone marrow (in vertaebra, pelvis, sternum, ribs, tiba, femor)

33
Q

What factor encouranges proliferation of neutrophils and supresses apoptosis in BM?

A

Granulocyte colony specific factor

34
Q

What causes anaemia through preduced production?

A

Stem cell defect - MDS, leukaemia, congenital
Erythroid hypoproliferation - CRF -> low EPO
Marrow inflitration - fibrosis, cells, cancer
Nutritional deficiency - iron, B12, folate

35
Q

What causes anaemia through increased loss?

A

Haemolysis - intrinsic : membrane issues, enzyme mutayions, thallasseamia
- extrinsic - immune, alloimmune, DIC, mechanical (heart valves)

Shortened lifespan - thallasaemia, MDS

Bleeding - obvious, occult, 3rd space

36
Q

How are iron supplements given?

A

Oral iron - ferrous sulphate 200mg

IV Iron - but no quicker at treating anaemia

37
Q

How can you alter iron absorption from the GI tract?

A

Increase absorption with:

  • low gastric pH - Converts iron into Fe2 - easier to absorb
  • Ascorbic acid
  • Anaemia

Decreased with:

  • Calcium/chelating drugs that bind iron
  • Wrong form of iron (eg. in cereals/tannins)
  • If Hb levels already ok
38
Q

If there is too much iron in the body, what can be used to reduce it? eg. repeted transfusion can cause overload

A

Iron chelators

  • Desferrioxamine IV - binds iron and excreted via kidneys
  • Deferasirox oral - excreted in faeces
39
Q

How can you rapidly increase iron levels?

A

Transfusion

40
Q

What is the ABO blood system?

A

A + B antigens can be present on RBC surface, genertically determined

If you have A/B/none you have the opposite antibodies in your plasma.

Blood type A - have B antibodies
Blood type AB - no antibodies
Blood type O - A and B antibodies

So determins who you can donate to and what blood you can receive.

41
Q

What is the Rhesus system of blood?

A

Rhesus D antigen is a surface protein

15% of caucasions are RhD -ve
If RhD -ve person is exposed to Rh +ve blood they can made anti-D IgG antibodies in response.

These can cross the placenta - so issue in pregnancy.

If They have Rh +ve baby, the IgG can cross placenta and destrol foetal red cells

-> haemolytic disease of newborn

42
Q

What can be given to try reduce the risks for a Rh -ve lady who has been exposed to Rh +ve blood?

A

Give them Anti-D, an IgM antibody

So it can’t cross placenta, but can mop up any Rh +ve blood in the body so you don’t produce your own IgG anti-D

43
Q

What is the Kleihauer test?

A

Identifies fetal blood cells present in the maternal blood - to help dose amount of anti-D needed to be given.

44
Q

Select the most appropriate disease mechanism for : Idiopathic thrombocytopenia

A Inherited abnormality of red cell enzyme function

B Clonal proliferation of platelet precursors (megakaryocytes) in the bone marrow

C Bone marrow infiltration by primitive myeloid precursors

D Immune suppression of marrow stem cells

E Constituitively activated tyrosine kinase

F Failure of B12 absorption

G Genetic mutation of haemoglobin genes

H Antibody mediated immune destruction of red cells by spleen

I Genetic mutation in red cell membrane proteins

J Drug induced haemolysis

K Antibody mediated immune destruction of platelets in the spleen

L Reduced erythroid maturation due to lack of erythropoietin

M Cytokine mediated bone marrow suppression

N Ineffective utilisation of iron

A

K Antibody mediated immune destruction of platelets in the spleen

45
Q

Select the most appropriate disease mechanism for : Hereditary spherocytosis

A Inherited abnormality of red cell enzyme function

B Clonal proliferation of platelet precursors (megakaryocytes) in the bone marrow

C Bone marrow infiltration by primitive myeloid precursors

D Immune suppression of marrow stem cells

E Constituitively activated tyrosine kinase

F Failure of B12 absorption

G Genetic mutation of haemoglobin genes

H Antibody mediated immune destruction of red cells by spleen

I Genetic mutation in red cell membrane proteins

J Drug induced haemolysis

K Antibody mediated immune destruction of platelets in the spleen

L Reduced erythroid maturation due to lack of erythropoietin

M Cytokine mediated bone marrow suppression

N Ineffective utilisation of iron

A

I Genetic mutation in red cell membrane proteins

46
Q

Select the most appropriate disease mechanism for : Aplastic anaemia

A Inherited abnormality of red cell enzyme function

B Clonal proliferation of platelet precursors (megakaryocytes) in the bone marrow

C Bone marrow infiltration by primitive myeloid precursors

D Immune suppression of marrow stem cells

E Constituitively activated tyrosine kinase

F Failure of B12 absorption

G Genetic mutation of haemoglobin genes

H Antibody mediated immune destruction of red cells by spleen

I Genetic mutation in red cell membrane proteins

J Drug induced haemolysis

K Antibody mediated immune destruction of platelets in the spleen

L Reduced erythroid maturation due to lack of erythropoietin

M Cytokine mediated bone marrow suppression

N Ineffective utilisation of iron

A

D Immune suppression of marrow stem cells

47
Q

Select the most appropriate disease mechanism for : Anaemia of chronic renal failure

A Inherited abnormality of red cell enzyme function

B Clonal proliferation of platelet precursors (megakaryocytes) in the bone marrow

C Bone marrow infiltration by primitive myeloid precursors

D Immune suppression of marrow stem cells

E Constituitively activated tyrosine kinase

F Failure of B12 absorption

G Genetic mutation of haemoglobin genes

H Antibody mediated immune destruction of red cells by spleen

I Genetic mutation in red cell membrane proteins

J Drug induced haemolysis

K Antibody mediated immune destruction of platelets in the spleen

L Reduced erythroid maturation due to lack of erythropoietin

M Cytokine mediated bone marrow suppression

N Ineffective utilisation of iron

A

L Reduced erythroid maturation due to lack of erythropoietin

48
Q

Select the most appropriate disease mechanism for : Thalassaemia

A Inherited abnormality of red cell enzyme function

B Clonal proliferation of platelet precursors (megakaryocytes) in the bone marrow

C Bone marrow infiltration by primitive myeloid precursors

D Immune suppression of marrow stem cells

E Constituitively activated tyrosine kinase

F Failure of B12 absorption

G Genetic mutation of haemoglobin genes

H Antibody mediated immune destruction of red cells by spleen

I Genetic mutation in red cell membrane proteins

J Drug induced haemolysis

K Antibody mediated immune destruction of platelets in the spleen

L Reduced erythroid maturation due to lack of erythropoietin

M Cytokine mediated bone marrow suppression

N Ineffective utilisation of iron

A

G Genetic mutation of haemoglobin genes

49
Q

Select the most appropriate description for the underlying disease mechanism for the following haematological conditions : Anaemia of chronic disease

A
Autoimmune suppression of bone marrow stem cells

H
Progressive red cell division due to inability to achieve optimum haemoglobin concentration

B Infiltration of bone marrow

I Lack of erythropoietin

C Cytokine induced suppression of marrow function

J Genetic abnormality of haemoglobin genes

D Immune destruction by the spleen

K Clonal abnormality of stem cells

E Infiltration by clonal proliferation of mature cells

L Genetic mutation causing constituitively activated tyrosine
kinase mediated clonal proliferation and reduced apotosis

F Lack of B 12

M Genetic abnormality of red cell membrane proteins

G Deficiency of iron

N Infiltration by clonal proliferation of
primitive cells

A

C Cytokine induced suppression of marrow function

50
Q

Select the most appropriate description for the underlying disease mechanism for the following haematological conditions : Acute lymphoblastic leukaemia

A
Autoimmune suppression of bone marrow stem cells

H
Progressive red cell division due to inability to achieve optimum haemoglobin concentration

B Infiltration of bone marrow

I Lack of erythropoietin

C Cytokine induced suppression of marrow function

J Genetic abnormality of haemoglobin genes

D Immune destruction by the spleen

K Clonal abnormality of stem cells

E Infiltration by clonal proliferation of mature cells

L Genetic mutation causing constituitively activated tyrosine
kinase mediated clonal proliferation and reduced apotosis

F Lack of B 12

M Genetic abnormality of red cell membrane proteins

G Deficiency of iron

N Infiltration by clonal proliferation of primitive cells

A

N Infiltration by clonal proliferation of primitive cells

51
Q

Microcytic hypochromic anaemia*(small pale red cells)

Select the most appropriate description for the underlying disease mechanism for the following haematological conditions :

A
Autoimmune suppression of bone marrow stem cells

H
Progressive red cell division due to inability to achieve optimum haemoglobin concentration

B Infiltration of bone marrow

I Lack of erythropoietin

C Cytokine induced suppression of marrow function

J Genetic abnormality of haemoglobin genes

D Immune destruction by the spleen

K Clonal abnormality of stem cells

E Infiltration by clonal proliferation of mature cells

L Genetic mutation causing constituitively activated tyrosine
kinase mediated clonal proliferation and reduced apotosis

F Lack of B 12

M Genetic abnormality of red cell membrane proteins

G Deficiency of iron

N Infiltration by clonal proliferation of primitive cells

A

H

Progressive red cell division due to inability to achieve optimum haemoglobin concentration

52
Q

Select the most appropriate description for the underlying disease mechanism for the following haematological conditions : Aplastic anaemia

A
Autoimmune suppression of bone marrow stem cells

H
Progressive red cell division due to inability to achieve optimum haemoglobin concentration

B Infiltration of bone marrow

I Lack of erythropoietin

C Cytokine induced suppression of marrow function

J Genetic abnormality of haemoglobin genes

D Immune destruction by the spleen

K Clonal abnormality of stem cells

E Infiltration by clonal proliferation of mature cells

L Genetic mutation causing constituitively activated tyrosine
kinase mediated clonal proliferation and reduced apotosis

F Lack of B 12

M Genetic abnormality of red cell membrane proteins

G Deficiency of iron

N Infiltration by clonal proliferation of primitive cells

A

A

Autoimmune suppression of bone marrow stem cells

53
Q

Select the most appropriate description for the underlying disease mechanism for the following haematological conditions : Chronic myeloid leukaemia

A
Autoimmune suppression of bone marrow stem cells

H
Progressive red cell division due to inability to achieve optimum haemoglobin concentration

B Infiltration of bone marrow

I Lack of erythropoietin

C Cytokine induced suppression of marrow function

J Genetic abnormality of haemoglobin genes

D Immune destruction by the spleen

K Clonal abnormality of stem cells

E Infiltration by clonal proliferation of mature cells

L Genetic mutation causing constituitively activated tyrosine
kinase mediated clonal proliferation and reduced apotosis

F Lack of B 12

M Genetic abnormality of red cell membrane proteins

G Deficiency of iron

N Infiltration by clonal proliferation of primitive cells

A

L Genetic mutation causing constituitively activated tyrosine
kinase mediated clonal proliferation and reduced apotosis

54
Q

Select the most appropriate description of the underlying disease mechanism for the following haematological diseases : Myeloma

A Lack of iron

H Suppression of marrow function by systemic cytokine release

B Bone marrow infiltration by reed sternberg cells, sclerosis and lymphocytes

I Infiltration of bone marrow by clonal proliferation of plasma cells

C Presence of a serum paraprotein

J Bone marrow stromal damage

D Presence of the Philadelphia chromosome

K Clonal proliferation and reduced apoptosis driven by constituitively activated tyrosine kinase

E Clonal abnormality of stem cells giving rise to infiltration of bone marrow by primitive myeloid precursors

L Reduced erythroid maturation due to lack of erythropoietin

F Autoimmune suppression of bone marrow stem cells

M Clonal abnormality of stem cells causing failure of functional development of all marrow cell lines

G Ineffective utilisation of iron

N Proliferation of mature myeloid precursors

A

I Infiltration of bone marrow by clonal proliferation of plasma cells

55
Q

Select the most appropriate description of the underlying disease mechanism for the following haematological diseases : Anaemia of renal failure

A Lack of iron

H Suppression of marrow function by systemic cytokine release

B Bone marrow infiltration by reed sternberg cells, sclerosis and lymphocytes

I Infiltration of bone marrow by clonal proliferation of plasma cells

C Presence of a serum paraprotein

J Bone marrow stromal damage

D Presence of the Philadelphia chromosome

K Clonal proliferation and reduced apoptosis driven by constituitively activated tyrosine kinase

E Clonal abnormality of stem cells giving rise to infiltration of bone marrow by primitive myeloid precursors

L Reduced erythroid maturation due to lack of erythropoietin

F Autoimmune suppression of bone marrow stem cells

M Clonal abnormality of stem cells causing failure of functional development of all marrow cell lines

G Ineffective utilisation of iron

N Proliferation of mature myeloid precursors

A

L Reduced erythroid maturation due to lack of erythropoietin

56
Q

Select the most appropriate description of the underlying disease mechanism for the following haematological diseases : Hodgkins disease

A Lack of iron

H Suppression of marrow function by systemic cytokine release

B Bone marrow infiltration by reed sternberg cells, sclerosis and lymphocytes

I Infiltration of bone marrow by clonal proliferation of plasma cells

C Presence of a serum paraprotein

J Bone marrow stromal damage

D Presence of the Philadelphia chromosome

K Clonal proliferation and reduced apoptosis driven by constituitively activated tyrosine kinase

E Clonal abnormality of stem cells giving rise to infiltration of bone marrow by primitive myeloid precursors

L Reduced erythroid maturation due to lack of erythropoietin

F Autoimmune suppression of bone marrow stem cells

M Clonal abnormality of stem cells causing failure of functional development of all marrow cell lines

G Ineffective utilisation of iron

N Proliferation of mature myeloid precursors

A

B Bone marrow infiltration by reed sternberg cells, sclerosis and lymphocytes

57
Q

Select the most appropriate description of the underlying disease mechanism for the following haematological diseases : Acute myeloid leukaemia

A Lack of iron

H Suppression of marrow function by systemic cytokine release

B Bone marrow infiltration by reed sternberg cells, sclerosis and lymphocytes

I Infiltration of bone marrow by clonal proliferation of plasma cells

C Presence of a serum paraprotein

J Bone marrow stromal damage

D Presence of the Philadelphia chromosome

K Clonal proliferation and reduced apoptosis driven by constituitively activated tyrosine kinase

E Clonal abnormality of stem cells giving rise to infiltration of bone marrow by primitive myeloid precursors

L Reduced erythroid maturation due to lack of erythropoietin

F Autoimmune suppression of bone marrow stem cells

M Clonal abnormality of stem cells causing failure of functional development of all marrow cell lines

G Ineffective utilisation of iron

N Proliferation of mature myeloid precursors

A

E Clonal abnormality of stem cells giving rise to infiltration of bone marrow by primitive myeloid precursors

58
Q

Select the most appropriate description of the underlying disease mechanism for the following haematological diseases : Myelodysplasia

A Lack of iron

H Suppression of marrow function by systemic cytokine release

B Bone marrow infiltration by reed sternberg cells, sclerosis and lymphocytes

I Infiltration of bone marrow by clonal proliferation of plasma cells

C Presence of a serum paraprotein

J Bone marrow stromal damage

D Presence of the Philadelphia chromosome

K Clonal proliferation and reduced apoptosis driven by constitutively activated tyrosine kinase

E Clonal abnormality of stem cells giving rise to infiltration of bone marrow by primitive myeloid precursors

L Reduced erythroid maturation due to lack of erythropoietin

F Autoimmune suppression of bone marrow stem cells

M Clonal abnormality of stem cells causing failure of functional development of all marrow cell lines

G Ineffective utilisation of iron

N Proliferation of mature myeloid precursors

A

M Clonal abnormality of stem cells causing failure of functional development of all marrow cell lines

Lucy Knox - Year 2.5 (15 decks)

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