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JMP Y2S1 > Week 30- overview of bone marrow > Flashcards

Week 30- overview of bone marrow Flashcards

1
Q

What are the most common single gene disorders?

A
  1. Thalassaemias

2. Haemoglobin variants

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2
Q

What are thalassaemias?

A

An imbalance of alpha and beta globin genes

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3
Q

How do haemoglobin variants come about?

A

A point mutation in an alpha or beta globin gene

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4
Q

How many haem molecules per rbc?

A

250mil

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5
Q

Where is the alpha globin cluster located and what subunits are produced there?

A

Chromosome 11

Alpha and zeta subunits

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6
Q

Where is the beta globin cluster located and what subunits are produced there?

A

Chromosome 16

Beta, gamma, delta and epsilon

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7
Q

What are the major control points in gene expression?

A

Major control points:

  1. Modification of DNA
  2. Transcription
  3. RNA processing/transport
  4. Translation
  5. Post-translational modification
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8
Q

What is an example of a genome level control for globin gene activity?

A

Activity inversely related to methylation of promoter region

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9
Q

How does the alpha globin mRNA remain stable?

A

Alpha complex interactions within its 3’UTR protects its polyA tail and prevents degradation

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10
Q

What is an example of a variant which affects alpha globin complex stability?

A

Part of the 3’UTR is translated:
Ribosome remains attached
Prevents alpha complex binding — shortening of polyA tail —leading to mRNA degradation

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11
Q

What is the cause of the clinical symptoms of thalassemias?

A

Normally characterised by a decrease in production of the affected globin protein.

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12
Q

What is the normal inheritance pattern of thalassemias?

A

Autosomal recessive

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13
Q

What are the different haemoglobin stages in development?

A
  1. Embryonic haemoglobin
  2. Foetal haemoglobin
  3. Adult haemoglobin
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14
Q

What can be said about the distribution for thalassemia variant distribution?

A

They can have geographic or ethnic clustering.

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15
Q

What is alpha thalassemia?

A

A disease characterised by on or more deletions of alpha-globin alleles

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16
Q

What is the normal make up of adult haemoglobin?

A

2 alpha and 2 beta globins (HbA)

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17
Q

What is the normal make up of foetal haemoglobin?

A

2 alpha 2 gamma (HbF)

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18
Q

How many alpha-globin alleles can someone have?

A

There is 4

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19
Q

What is the 4 types of alpha thalassemias?

A

Between 1-4 deletions of the alpha-globin alleles:
1 deletion = silent carrier
2 deletions = alpha thalassemia trait
3 deletions = Haemoglobin H (HbH) disease
4 deletions = Hydrops fetalis

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20
Q

What is the effects of a 1 deletion alpha thalassemia?

A

No effect —> silent carrier

Only very minimal decrease in alpha globin production

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21
Q

What is the effect of a 2 deletion alpha thalassemia?

A
  1. Decreased aloha globin production-Normal beta globin production
  2. Reduced HbA formation (adult haemoglobin)
  3. No significant excess of Beta globin
  4. Occasional finding of HbH (excess Beta globin unstable binds to form this)
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22
Q

What is the effect of a 3 deletion thalassemia?

A
  1. Larger decrease in alpha globin production - normal beta globin production
  2. Reduced alpha globin production reduces HbA formation and hence leaves lots of free beta globin.
  3. Beta globin unstable binds together to form unstable HbH (B4)
  4. HbH inclusion bodies obvious via microscopy
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23
Q

What is the effect of a 4 deletion thalassemia?

A
  1. No alpha globin production
  2. Fetes relies on foetal haemoglobin to take maternal O2 (HbF)
  3. No alpha production but there is normal gamma globin production
  4. Gamma globin forms (Gamma 4) —> G4 has an extremely high oxygen affinity that it does not allow for O2 release at tissues
  5. Foetal death results from hypoxia and heart failure.
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24
Q

What are some forms of Beta thalassemias?

A
  1. Beta0 —> absence of beta chain production

2. Beta+ —> reduction of beta chain production

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25
Q

How does Beta0 thalassemias normally arise?

A 
Deletion mut
Initiation codon mut
Nonsense mut
Frameshift mut
Splicing mut
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26
Q

How do Beta+ thalassemias normally arise?

A 
Promoter area
Polyadenylation signal’
5’ or 3’ UTR 
Splicing abnormalities 
May be severe mild or silent
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27
Q

What causes sickle cell anaemia?

A

Change in beta globin amino acid sequence

Normally glutamic acid —> changed to valine

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28
Q

What is the effect of sickle cell anaemia?

A

Haemoglobin molecules crystallise when O2 concentrations are low —> causing RBC to sickle in shape and get stuck in small vessels

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29
Q

What is the distribution of sickle cell and malaria diseases?

A

Africa and some of asia

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30
Q

What is a benefit of having sickle cell disease?

A

Sickle Hb confers tolerance to plasmodium infections

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31
Q

What is the inheritance pattern of sickle cell?

A

Autosomal recessive

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32
Q

What is the most common genetic disorder in Australia?

A

Haemochromatosis (autosomal recessive pattern)

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33
Q

What is haemochromatosis?

A

A disorder of iron overload

Affected people absorb too much iron from their diet

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34
Q

What is the formation of blood cells known as?

A

Haemopoiesis

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35
Q

What is the difference between haematopoiesis and haemopoiesis?

A 
Haemato = process in which blood cells are produced
Haemo = formation of new cellular components of the blood in myeloid and lymphoid tissue
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36
Q

In adults where is all blood cells produced?

A

Red bone marrow

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37
Q

Where is red bone marrow located?

A

restricted to the bones of the axial skeleton-vertebrae, ribs, sternum, skull, sacrum, pelvis and proximal femora

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38
Q

What is the composition of bone marrow in the regions of red bone marrow?

A

50% fat —> 50% blood cells + precursors.

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39
Q

Can other bones in the body contribute to blood cell production (Haemopoiesis)?

A

Yes –> Fatty marrow in other bones can be used in times of increased demands of blood cells in some diseases

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40
Q

What is the origin of all blood cells?

A

A single pluripotent cell known as the haemocytoblast

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41
Q

Where is blood cells developed in foetal vs adult?

A

Foetal blood cells from yolk sac, liver, spleen

Adult —> flat bone marrow

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42
Q

What are the two main branches of the haemocytoblast?

A

Common lymphoid progenitor (CLP)

Common myeloid progenitor (CMP)

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43
Q

What does the CLP further branch into?

A
  1. Pre B and pre T cells
  2. B and T lymphoblasts
  3. B and T lymphocytes
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44
Q

What does the CMP further branch into?

Two main branches:

A

Granulocyte- monocytes progenitor and Megakaryocyte erythroid progenitor

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45
Q

What does the granulocyte monocytes progenitor branch and end at?

A

Basophil, neutrophil, eosinophils, monocytes

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46
Q

What does the Megakaryocyte erythroid progenitor branch and end?

A

Megakaryoblast —> Megakaryocyte —> platelets

Pronormablast —> Normablast —> Erythrocytes

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47
Q

What are the main cell types in the peripheral blood and their corresponding precursor?

A
  1. T-cells —> pre T cells
  2. B-cells —> pre B cells
  3. RBC —> Normablast
  4. Megakaryocyte/Platelet —> Megakaryoblast
  5. Granulocyte — granulocyte - monocyte progenitor
  6. Monocytes —> granulocyte - monocyte progenitor
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48
Q

What is the protein responsible for blood type?

A

Agglutinogens

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49
Q

How many combinations of blood types are their?

A

3 alleles —> 2 parents —> 6 combinations

A, B, O, AB, AO, BO

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50
Q

What is the Rhesus factor?

A

A blood protein that is either present or not. (Rh + vs Rh-)

Can impact blood products received.

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51
Q

What blood groups can A type receive?

A

A and O can receive like blood and O

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52
Q

What blood groups can AB receive?

A

—> all

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53
Q

What is the size of an erythrocytes and how small is a capillary?

A

RBC –> 8uM

Capillary is 3uM —> RBC bends to squeeze through

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54
Q

What type of iron is required for haem?

A

Fe2+ Not 3+

55
Q

Define anaemia?

A

Reduction in the number of circulating erythrocytes and therefore haemoglobin, reducing the capacity of blood to carry oxygen.

56
Q

What is the mechanisms leading to anaemia?

A

Loss of RBC production
Loss of blood volume
Increase in erythrocyte destruction
(OR COMBINATION OF THESE)

57
Q

What are some common causes of Loss of RBC production anaemia?

A
  1. Lack of nutrition —> iron, B12, folic acid
  2. Increased requirements —> adolescence, pregnancy
  3. Iron retention —> cancer, chronic infection, inflammation
  4. Failure of bone marrow —> apoplastic anaemia, acute leukaemia
  5. Reduced EPO —> eg kidney disease, thyroid?
58
Q

What are some causes of increased red cell destruction anaemias?

A
  1. Intrinsic red cell defect —> hereditary spherocytosis, enzyme deficiencies, thalassemias
  2. Extrinsic factors —> AIHA, microcirculation abnormalities
59
Q

What are some causes of increased red cell loss anaemias?

A

Haemorrhage, parasites

60
Q

What are the prefixes for aneamia to classify based on cell size?

A

Micro —> small cells
Normo —> normal sized cells
Macro —> large cells

61
Q

What are some suffixes that can be used to describe anaemia?

A

Chromic —> colour —> eg hypochromic (light), hyperchromic (dark)
Cytic —> just means cell —> eg macrocytic = large cells

62
Q

Causes of microcytic anaemia?

A
  1. Defect in haem synthesis —> iron deficiency, chronic disease
  2. Defect in globulin synthesis —> alpha or Beta chain synthesis issues (thalassemias)
63
Q

Causes of Normocytic anaemia?

A
  1. Haemorrhage —> can be things like peptic ulcers, varices, etc
  2. Chronic renal failure
  3. Haemolytic anaemia
  4. Red cell pooling in spleen
  5. Rbc production failure
  6. Early stages of iron deficiency anaemia or chronic disease
  7. Bone marrow failure/suppression
  8. Bone marrow infiltration
  9. Hypersplenism (gets from portal cirrhosis
64
Q

Causes of Macrocytic anaemia?

A

Normally from abnormal haemopoiesis —> RBC precursors continue to produce haem and cellular proteins but have issues dividing properly —> hence larger

  1. Vit B12 deficiency
  2. Pernicious anaemia
  3. Leukemias
  4. Liver disease and ethanol toxicity
  5. Recent major blood loss with adequate iron stores (reticulocytes increased)
  6. Haemolytic anaemia (reticulocytes increased)
65
Q

What are reticulocytes?

A

Immature erythrocytes (RBCs)

66
Q

What does pernicious anaemia mean?

A

Pernicious anaemia is where the body cannot absorb Vit B12 and hence RBC production is non functioning –> large immature RBC circulate the blood and are non functioning

67
Q

What are some causes of haemolytic aneamia?

A
  1. Intrinsic—> inherited factors that accelerate RBC degradation
  2. Extrinsic —> microorganisms, drugs, chemicals
68
Q

What are the two classifications of haemolytic?

A
  1. Intravascular—> occurs if there is acute RBC damage

2. Extravascular —> occurs when defective RBC are removed by the spleen

69
Q

What is polycythaemia?

A

Too many RBCS in circulation

70
Q

What causes pseudo polycythaemia

A

Reduced blood volumes —> give signs of polycythemias but are classified as pseudo.

71
Q

True causes of polycythaemias?

A
  1. Too much blood—> over transfusing
  2. Too much EPO —> increases RBC production
  3. Abnormal bone marrow function
72
Q

What results can polycythemia have?

A

Hyperviscosity

Hypertension

73
Q

What is leucocytosis?

A

Higher than normal white cells —> sign of inflammation, most commonly infection but can be due to parasites, bone tumours or leukaemia.

74
Q

What is neutropenia?

A

Lack of neutrophils in the blood —> a type of white blood cell important for first line immune defence.

75
Q

How is abnormal White cell count investigated?

A
  • History and examination
  • Haemoglobin and platelet count
  • Automated differential
  • Examine blood film
76
Q

What too consider when assessing a white cell abnormality?

A
  • Abnormality -White cells only, or all 3 lineages (red cells/platelets/white cells) ? •White cells 1 cell type only, or all lineages? (e.g. neuts/eos/monocytes/lymphocytes)
  • Mature cells only or mature and immature cells?
77
Q

Common causes for rise in neutrophils?

A
  1. Infection
  2. Tissue inflammation
  3. Physical stress —> adrenaline, corticosteroids
  4. Neoplasia
78
Q

Common causes for rise in eosinophils?

A

Parasitic infection

Allergic disease eg Asthma

79
Q

Common causes for rise in lymphocytes?

A

Infection (bacterial, viral, other)
Cancer of the blood or lymphatic system
An autoimmune disorder causing ongoing (chronic) inflammation

80
Q

What is a reactive lymphocyte?

A

Normal haematopoiesis —> polyclonal/ reactive

81
Q

What is a malignant lymphocyte?

A

Abnormal/clonal —> eg leukaemia

82
Q

How is haematopoiesis disturbed in cancers like leukemia, myeloma, lymphoma?

A

Mutation of single stem cell.
Neoplastic proliferation of lymphoid tissue (lymphoma)
B-cell neoplasticism growth (myeloma)

83
Q

Cross- sectional study design?

A

Cross-sectional study designis a type of observationalstudy design. In across-sectional study, the investigator measures the outcome and the exposures in thestudyparticipants at the same time.

84
Q

Purpose of a cross sectional study?

A

Cross-sectional studiesinvolve data collected at a defined time. They are oftenusedto assess the prevalence of acute or chronic conditions, but cannot beusedto answer questions about the causes of disease or the results of intervention.

85
Q

Case control study design?

A

Acase-control studyisdesignedto help determine if an exposure is associated with an outcome

86
Q

Purpose of a case control study?

A

Thecase–control studydesign is often used in thestudyof rare diseases or as a preliminarystudywhere little is known about the association between the risk factor and disease of interest.

87
Q

Cohort study design?

A

A study design where one or more samples (called cohorts) are followed prospectively and subsequent status evaluations with respect to a disease or outcome are conducted to determine which initial participants exposure characteristics (risk factors) are associated with it.

88
Q

Purpose of a cohort study?

A

Cohort studiesare a type of medicalresearchused to investigate the causes of disease and to establish links between risk factors and health outcomes.

89
Q

What are the two types of cohort study?

A

Prospective –> monitoring a cohort going forward

Retrospective –> monitoring a cohort is a historical cohort context

90
Q

What is the design of interventional studies?

A

Aninterventional studyis one in which the participants receive some kind ofintervention, such as a new medicine, in order to evaluate it.

91
Q

What is the purpose of interventional studies?

A

to test efficacy of specific treatments or combination treatments

92
Q

What is the design of qualitative studies?

A

Aqualitative research designis concerned with establishing answers to the whys and hows of the phenomenon in question (unlike quantitative). Due to this,qualitative researchis often defined as being subjective (not objective), and findings are gathered in a written format as opposed to numerical.

93
Q

What is the purpose of qualitative studies?

A

Qualitative researchis aimed at gaining a deep understanding of a specific organization or event, rather a than surface description of a large sample of a population

94
Q

What is the design of systematic reviews?

A

Systematic reviewsare a type of literaturereviewthat usessystematicmethods to collect secondary data, critically appraiseresearchstudies, and synthesize findings qualitatively or quantitatively.

95
Q

What is the purpose of systematic reviews?

A

to deliver a meticulous summary of all the available primaryresearchin response to aresearchquestion.

96
Q

Where is iron absorbed in the body?

A

The duodenum

97
Q

How is iron absorbed?

A

Gastric acid lowers the pH in the proximal duodenum, enhancing the solubility and uptake of ferric iron

98
Q

How is iron transported?

A

Transferrin is the majoriron transportprotein (transportsironthrough blood). Fe3+ is the form ofironthat binds to transferrin, so the Fe2+transportedthrough ferroportin must be oxidized to Fe3+. … Once oxidized, Fe3+ binds to transferrin and istransportedto a tissue cell that contains a transferrin receptor.

99
Q

What is the effect of low iron on RBC production?

A
  1. Limits the production of haem
  2. Low haem limits production of RBC haemoglobin
  3. Low haemoglobin reduces bloods capacity to carry oxygen
100
Q

How does low folate and or B12 affect RBC production?

A

Deficiency of folate or vitamin B12 inhibits purine and thymidylate syntheses, impairs DNA synthesis, and causes erythroblast apoptosis, resulting in anaemia from ineffective erythropoiesis (RBC production)

101
Q

What is the structure of haemoglobin?

A

Haemoglobinis a globular protein with a quaternarystructure.
Consists of four polypeptide subunits –> 2 alpha chains and 2 beta chains.

102
Q

What is the function of haemoglobin?

A

Oxygen transporting protein of RBCs

103
Q

What is the three main hormones involved in the renin system for blood pressure regulation?

A
  1. Renin
    1. Angiotensin 2
    2. Aldosterone
104
Q

What impacts renin release from the kidneys?

A
  1. Reduced NaCl delivery to the distal tubule of the macula densa
  2. Reduced perfusion pressure in the kidney
  3. Sympathetic stimulation of the Juxtaglomerular apparatus (JGA)
105
Q

What is the general flow of mechanisms in the Angiotensin renin system?

A
  1. Renin release
  2. Renin cleaves Angiotensin to form Angiotensin 1
  3. Angiotensin 1 is converted to angiotensin 2 by angiotensin converting enzymes (ACE)–> these are found mainly in the lungs and renal and capillary endothelium
  4. Angiotensin 2 has numerous sites of action:
    - Adrenal cortex –> stimulates the production of aldosterone (stimulates Na+ and subsequently water reabsorption)
    - Cardiovascular –> acts on AT1 receptors in arterioles to drive vasoconstriction
    - Neural –> hypothalamus action to stimulate thirst
106
Q

How does the baroreflex (baroreceptor reflex) have effect?

A
  1. Baroreceptors (stretch sensitive mechanoreceptors in the atria, vena cavae and most importantly the carotid sinuses and aortic arch
  2. When stretch is detected –> signals trigger vagal nuclei
  3. Sympathetic nervous system is inhibited and parasympathetic is activated
  4. Decreased cardiac output via decrease in heart rate, resulting in a tendency to lower blood pressure.
  5. NOTE –> the baroreflex can have the opposite action to increase BP via sympathetic activation
107
Q

What does sympathetic activation do to the heart and vasculature?

A

Heart –> stimulate

Vasculature –> constrict

108
Q

What does parasympathetic activation do to the heart and vasculature?

A

Heart –> inhibition

Vasculature –> dilation

109
Q

What increases RBC formation in bone marrow?

A

EPO –> released in the kidneys in response to hypoxia

110
Q

What stimulates white blood cell formation in the bone marrow?

A

Infection mediators

111
Q

What increases platelet formation in the bone marrow?

A

Thrombopoietin is a glycoprotein hormone produced by the liver and kidney which regulates theproductionofplatelets. Itstimulatestheproductionand differentiation of megakaryocytes, the bone marrow cells that bud off large numbers ofplatelets.

112
Q

What is haemolysis?

A

The lysis of RBCs

113
Q

What is the common causes of haemolysis?

A 
Extrinsic:
1. Infection
2. Tumour
3. Autoimmune disorder
4. Medication
5. Leukemia
6. Lymphoma
Intrinsic:
1. Sickle cell anaemia
2. Thalassemia
114
Q

What are the general symptoms of anaemia?

A
  1. Fatigue, energy loss
  2. SOB with exercise
  3. Dizziness
  4. Pale skin, nail beds, palms
  5. Fast heart rate
  6. Cramps
115
Q

What are some symptoms of iron deficiency anaemia?

A
  1. Koilonychias (upward curvature of the nails
  2. Soreness of the mouth with cracks in the corners
  3. Pica –> strange food cravings
116
Q

What are some particular symptoms of B12 deficiency anaemia?

A
  1. Tingling in hands or feet
  2. Wobbly gait
  3. –> neurological issues (touch, stiffness, dementia)
117
Q

What are some symptoms of haemolytic anaemia?

A
  1. Jaundice
  2. Brown/red urine
  3. Leg ulcers
  4. Gallstone symptoms
  5. Failure to thrive in infants
118
Q

What is the typical clinical presentation of someone with sickle cell disease?

A

Usually at about 5months of age:

  1. Anaemia related fatigue
  2. Episodes of pain –> when sickle cells block blood vessels
  3. Swelling of hands and feet –> from sickle cell blockages
  4. Frequent infections –> as sickle cells damage the spleen
  5. vision problems –> eye vessels get blocked by sickle cells
119
Q

What are some symptoms of thalassaemia’s?

A

Usually shows up later in childhood or adolescence

  1. Dark urine
  2. Delayed growth/development
  3. Excessive fatigue
  4. Yellow/pale skin
  5. Bone deformities in the face
120
Q

What does anaemia look like under the microscope?

A
  1. Size of the cells can classify anaemia (Micro, normo, and macrocytic)
  2. Colour can classify anaemia (hyper/hypo chromic)
121
Q

How does flow cytometry work?

A

In this process, a sample containing cells or particles is suspended in a fluid and injected into the flow cytometer instrument. The sample is focused to ideally flow one cell at a time through a laser beam, where the light scattered is characteristic to the cells and their components.

122
Q

What is RBC mean on a FBC?

A

The number of red blood cells

123
Q

What is HGB on a FBC?

A

Haemoglobin levels

124
Q

What is HCT on FBC?

A

Haematocrit –> ratio of red blood cells to total blood volume

125
Q

What is MCV on FBC?

A

mean corpuscular volume (mean cell volume) –> determines the average size of the RBCs –> can show if micro, normo or macrocytic

126
Q

What is MCH on FBC?

A

Mean cell haemoglobin –> average NUMBER of haemoglobin inside a RBC
–> these values can be seen to be higher in macrocytic cells as they have more volume and the opposite for microcytic

127
Q

What is MCHC on FBC?

A

Mean cell haemoglobin concentration –> CONCENTRATION of haemoglobin in RBC

  • -> can determine hyper or hypochromic cells
  • -> will be lower in iron deficiency anaemias and thalassaemia’s
128
Q

What is RDW on FBC?

A

Red cell distribution width –> calculation of cell size variation of RBCs
–> RDW is commonly higher in some anaemias such as pernicious (B12) (more immature cells which are actually larger than mature cells

129
Q

What does serum iron measure in iron studies?

A

Measures iron levels in liquid blood

130
Q

What does ferritin measure in iron studies?

A

Measures amounts of stored iron in the body

131
Q

What does transferrin (TIBC) measure in iron studies?

A

Total iron binding capacity –> shows how much spare capacity the circulation has to transport iron. It is equal to the amount of non-bonded transferrin (iron transport protein) + serum iron.

132
Q

What does transferrin saturation measure in iron studies?

A

The saturation levels of transferrin –> represented as a percentage

133
Q

What does soluble transferrin receptor measure in iron studies?

A

Levels of transferrin receptor (iron binding capacity in blood) –> is normally elevated in iron deficiency anaemia

134
Q

What are the common deliver methods of iron to patients?

A
  1. Dietary change
  2. Supplements
  3. Iron injection intramuscular
  4. Infusion
  5. Transfusion

JMP Y2S1 (24 decks)

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