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Medicine Phase 2A (OWN) > Haematology > Flashcards

Haematology Flashcards

1
Q

Give the reticulocyte percentage in RBC underproduction compared to destruction

A

<3% in underproduction as decreased bone marrow response

>3% in destruction as increased bone marrow activity

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2
Q

What does MCV stand for and what should it be for a normal RBC/ in normocytic anaemia?

A

Mean corpuscular volume = 80-100 micro meters cubed

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3
Q

What is the MCV in macrocytic anaemia?

A

> 100

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4
Q

What is the MCV in microcytic anaemia?

A

<80

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5
Q

What causes microcytic anaemia?

A

Decrease in haemoglobin which leads to the splitting of RBCs in order to try and increase haemoglobin concentration

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6
Q

Give the 4 general causes of Iron deficiency anaemia

A

Decreased intake
Increase in the body’s demand
Decrease in absorption
Increase in blood loss

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7
Q

Why might someone’s intake of iron decrease?

A

Infants <6 months, generally feed on breast milk which lacks iron

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8
Q

Why might the body’s demand for iron increase?

A

Child/ adolescent- growing

Pregnant women

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9
Q

Why might there be a decrease in iron absorption?

A

Decrease in production of stomach acid if patient is on a PPI or has had a gastrectomy
Problem in the duodenum- Coeliac disease

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10
Q

Why might there be an increase in blood loss leading to anaemia?

A

Heavy menstruation
Peptic ulcer disease
Hookworm infection
Colon cancer/ polyps

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11
Q

How might you diagnose iron deficiency anaemia?

A 
Symptoms of anaemia
As well as:
Koilonychia- spoon shaped nails 
Pica- desire to eat inedible things
Restless leg syndrome
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12
Q

How is iron transported and stored in the body?

A

Iron binds to transferrin in the blood

Iron binds to ferritin in the liver and is stored in macrophages (Kupffer cells)

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13
Q

How are ferritin and transferrin levels affected in iron deficiency anaemia?

A

Ferritin decreases

Transferrin increases in order to compensate for iron loss and increase total iron binding capacity

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14
Q

What type of anaemia is anaemia of chronic disease?

A

Microcytic

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15
Q

What is hepcidin and how do levels vary in relation to iron levels?

A

A major iron regulator
When iron levels decrease, hepcidin decreases
When iron levels increase, hepcidin increases
This is because hepcidin decreases serum iron

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16
Q

How does hepcidin decrease serum iron?

A

It blocks ferroportin channels, inhibiting the passage of iron across duodenal cells/ absorption from the gut

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17
Q

What is the consequence of hepcidin preventing degration of RBCs after 120 days?

A

Iron cannot be released and saved/ recycled

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18
Q

Why is hepcidin released in response to an inflammatory disease?

A

Iron can be a key nutrient needed for bacterial growth so hepcidin is released in response to cytokines so that iron levels decrease

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19
Q

Give the potential treatments for Iron deficiency anaemia

A

Oral iron supplements- taken with an acidic drink (this can cause black stools)
IV iron
Blood transfusion
- With increased blood loss or decreased absorption supplements are not enough

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20
Q

Why would you not treat anaemia of chronic disease with iron?

A

May increase the rate of bacterial growth

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21
Q

Describe the mechanism of microcytic anaemia

A

Between G2 and M phase, reticulocytes grow too big and haemolysis occurs as a result

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22
Q

What is the compensatory mechanism that occurs as a result of macrocytic anaemia?

A

Bone marrow hyperplasia in order to increase reticulocytes

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23
Q

Give the causes of macrocytic anaemia

A 
Folate deficiency (THF)
B12 deficiency
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24
Q

How does folate deficiency lead to macrocytic anaemia?

A

THF converts to purines through a number of reactions, specifically adenine and guanine
Therefore a deficiency in folate means that DNA is not synthesised correctly

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25
Q

Give 3 causes of B12 deficiency

A

Resection of terminal ilium
Tapeworm
Lack of intrinsic factor- this is pernicious anaemia

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26
Q

Which cells produce intrinsic factor?

A

Parietal cells

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27
Q

Give the treatment of folate deficiency and B12 deficiency

A

Folate: oral folic acid
B12: Parenteral B12

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28
Q

Which drugs inhibit the conversion of folic acid to THF?

A

Methotrexate
AVT
Cyclophosphamide
Trimethoprim

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29
Q

Which type of haemoglobin is affected in sickle-cell disorder?

A

Haemoglobin A
2 alpha globin
2 beta globin

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30
Q

Describe what is meant by heterozygote advantage in sickle cell anaemia

A

Sickle trait (carrier)
No health problems unless exposed to extreme conditions
Decreases the severity of P. falciparum malaria

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31
Q

Describe the mutation that occurs in sickle cell anaemia

A

Non-conservative missense mutation
Glutamic acid (hydrophilic) is replaced with Valine (hydrophobic)
Sickle cell haemoglobin with mutated beta globin is called HbS

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32
Q

How do HbS form the sickle shape?

A

When deoxygenated, it changes shape allowing it to aggregate with other HbS proteins and form long polymers in a sickle shape

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33
Q

Give two conditions that promote sickling

A

Acidosis as this decreases Hb affinity for oxygen

Low flow vessels as Hb has time to dissociate from lots of oxygen

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34
Q

How can repeated sickling cause scleral icterus, jaundice and gallstones?

A

Repeated sickling leads to weakened cell membranes and therefore premature destruction where Hb spills out
Recycled haptoglobin yields unconjugated bilirubin

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35
Q

What is the effect of an increased production of reticulocytes by the bone marrow in anaemia?

A

New bone formation as increased activity of bone marrow

Expansion of medullar cavities in skull causing enlarged cheeks

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36
Q

Describe extra medullary hematopoiesis and what this causes

A

In anaemia there may be RBC production outside the bone marrow which travel to the liver and cause hepatomegaly

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37
Q

What happens when sickle cells clog blood flow in infants?

A

Obstruct supply to hands and feet causing dactylitis in infancy

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38
Q

What happens when sickle RBCs clog up the spleen?

A

Infarct leading to autosplenectomy (fibrosis) and splenic sequestration
The patient is therefore susceptible to encapsulated bacteria since encapsulated bacteria are usually opsonised and phagocytised by macrophages in the spleen

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39
Q

What can occur if sickle cells become stuck in cerebral vasculature?

A

Stroke

Moya-moya disease- “puff of smoke” collateral vessels that bypass blocked arteries

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40
Q

What can occur if sickle cells become stuck in the vessels of the following organs:
Lungs
Kidneys
Penis

A

Lungs: acute chest syndrome
Kidneys: Necrosis leading to haematuria and proteinuria
Penis: priapism- painful and prolonged erection

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41
Q

How would you diagnose sickle cell anaemia?

A

Newborn blood spot screen
Blood smear
Protein electrophoresis

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42
Q

How would you treat sickle cell anaemia?

A

Oxygen and fluids
Opioids to manage pain
Abx to treat underlying bacterial infection from acute chest syndrome
Blood transfusion
Hydroxyurea- increases alpha globin and HbF (no beta globin so no mutation), which gets in the way of HbS
Bone marrow transplant
Gene therapy

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43
Q

Describe the process of DVT formation

A

Damage to endothelium
Vasoconstriction
Platelets: adhere, are activated by collagen and tissue factor, recruit more forming a plug
Clotting factors are activated, terminally activating fibrinogen to convert to fibrin forming a mesh over the platelet plug
This plaque can break off and form a clot

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44
Q

Give the three factors of Virchow’s triad that lead to DVT

A

Slowed blood flow
Hypercoagulation (genetics, surgery, medications)
Damage (Infections, chronic inflammation, tobacco smoke)

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45
Q

Describe the symptoms and diagnosis of DVT

A

Symptoms:
Pain, swelling, redness, warm

Diagnosis:
US, Venography, D dimer blood test

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46
Q

Define acute leukemia

A

The precursor “blasts” can’t differentiate any further, normally % of blasts in bone marrow is 1-2 %
In leukaemia it is >20%

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47
Q

What is the effect of an increased number of precursor cells in the bone marrow in leukaemia?

A

Cytopoeina as normal cells are “crowded out”
Anaemia: fatigue
Thrombocytopenia: bleeding
Neutropenia: Infection

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48
Q

How would you test for lymphoblasts?

A

TdT positive

49
Q

How do you differentiate between B-ALL and T-ALL?

A

B- expresses surface markers CD10, 19 and 20

T- expresses surface markers CD2-CD8

50
Q

How would you test for myeloblasts?

A

Auer rods

Positive myeloperoxidase seen via cytoplasmic staining

51
Q

What is the Philadelphia chromosome and how does it affect prognosis in leukaemia?

A

t(9;22) Ph +ve

Poor prognosis

52
Q

How would you classify acute myeloid leukaemia by lineage?

A

Mono blast AML
Megakaryoblast AML
Erythroblast AML

53
Q

Which type of leukemias are associated with Down’s syndrome and at what age?

A

0-5 years- megakaryoblastic leukaemia

>5 years- acute lymphoblastic lymphoma

54
Q

Give 2 conditions that can lead to AML

A

Myelodysplastic syndrome- blast build up in bone marrow

Myelodysplasia- poor formation of bone marrow cells

55
Q

What is the most common cause of leukaemia?

A

Chromosomal abnormality in haematopoietic stem cells which will affect leukocytes so that they only mature partially and don’t work effectively

56
Q

Describe the difference between chronic myeloid and chronic lymphocytic leukaemia

A

CML:
Affects granulocytes
Cells divide too quickly

CLL:
Affects lymphocytes
Cells don’t die when they should

57
Q

How can chronic leukaemia progress to acute leukaemia?

A

More divisions leads to increased mutations

This progression is often caused by trisomy of chromosome 8 or doubling of Philadelphia chromosome

58
Q

Describe the mechanism of chronic lymphocytic leukaemia

A

Mutations interfere with B cell receptors which should only be signalled during inflammation
Excess B cells in the bone marrow are forced into the blood and lymphatic system leading to lymphadenopathy
This is a lymphoma

59
Q

Give 5 symptoms of chronic leukaemia

A

Fatigue
Easier bleeding
More infections
In CML hepatosplenomegaly- feeling of fullness
In CLL lymphadenopathy- pain in the lymph node

60
Q

How would you diagnose CML?

A

Increased granulocytes and monocytes in blood smear

61
Q

How would you diagnose CLL?

A

Smudge cells- immature B cells, broken during smear in blood smear

62
Q

How would you treat chronic leukaemia?

A

Biological therapy: tyrosine kinase inhibitor (less effective for CLL)
Chemo
Stem cell transplant
Bone marrow transplant

63
Q

What is the key feature of non-Hodgkin lymphoma?

A

Absence of Reed-Sternberg cell

64
Q

Describe the differentiation of B cells in lymph nodes

A

B cells grouped into follicles in the cortex of lymph nodes
Some differentiate directly into plasma cells and produce IgM antibodies
Memory B cells travel to the blood, lymph nodes, spleen and mucosa-associated lymphoid tissue

65
Q

Describe the mechanism of non-Hodgkin lymphoma

A

A genetic mutation occurs where cells which should usually undergo apoptosis instead divide uncontrollably forming nodal lymphomas

66
Q

How does NHL affect the following:
GI tract
Bone marrow
Spinal cord

A

GI: Bowel obstruction
Bone marrow: crowds out normal cells
Spinal cord: spinal cord compression

67
Q

Give 4 general symptoms of lymphoma

A

Painless lymphadenopathy
Fever
Night sweats
Weight loss

68
Q

How would you diagnose lymphoma?

A 
Imaging studies (CT scan) to establish stage
Lymph node biopsy
69
Q

How would you treat lymphoma?

A

Chemo/ radiation therapy

If CD20 +ve rituximab can be used to induce complement-mediated lysis as well as direct cytotoxicity and apoptosis

70
Q

What is multiple myeloma?

A

Malignant disease of plasma cells in the bone marrow

71
Q

What differences can be seen in the bone marrow of someone with multiple myeloma?

A

> 10% plasma cells

Producing abnormal antibodies and only light chains produced (paraproteins)

72
Q

Give 5 symptoms of multiple myeloma

A 
Back pain
Lytic bone lesions
Anaemia
Dehydration
Infections
Fractures
Renal failure
Proteinuria
73
Q

Give the three types of bone cells

A

Osteoblasts
Osteoclasts
Bone marrow stroll cells- regulate haematopoeisis

74
Q

Which immunoglobulins are produced in high amounts in multiple myeloma?

A

IgG and IgA

75
Q

How do osteoclasts break down bone?

A

Releasing HCl

76
Q

What do osteoblasts release in order to build bone?

A

Osteoid and minerals (calcium and phosphate)

77
Q

How is osteoclast activation regulated by osteoblasts?

A

Rank on osteoclasts binds to rank ligand on osteoblasts

78
Q

How do bone marrow stromal cells help myeloma cells survive and grow?

A

Adhesion of bone marrow cells to myeloma cells stimulates cytokine mediated growth, survival, drug resistance and migration

79
Q

What is osteoprotegerin?

A

It inhibits the differentiation of osteoclast precursors

80
Q

How do multiple myeloma cells reduce osteoblast activity?

A

Release IL-3 which inhibits osteoblast progenitor cells

81
Q

How do multiple myeloma cells increase osteoclast activity?

A

Release DKK1 which inhibits OPG

Expression of rank ligand

82
Q

What are the problems caused by hypercalcaemia as a result of multiple myeloma?

A

Nerve problems

Dehydration

83
Q

What are the problems caused by paraproteinaemia in multiple myeloma?

A

Can pass through the glomerulus and cause renal failure

84
Q

What is the name for the light chain proteins in the urine in multiple myeloma?

A

Bence-Jones proteins

85
Q

Why do you get anaemia from multiple myeloma?

A

Shift from myeloid to lymphoid progenitor to make more plasma cells
Over-production of plasma cells clogs up bone marrow
Kidney failure- decreased erythropoiesis, so decreased RBC production

86
Q

What would be the results of a blood and urine test in multiple myeloma?

A 
Anaemia
Paraproteinaemia
Decrease in normal antibodies 
Hypercalcaemia
Increase in urea and nitrogenous bases- renal failure
Increase in creatinine 
Bence- Jones proteins in urine
87
Q

What bone investigations would you carry out for multiple myeloma?

A 
Bone aspiration
Bone marrow biopsy
X-ray
CT scan- lesions of bone and soft tissue
MRI
88
Q

How would you diagnose multiple myeloma?

A 
Monoclonal plasma cell in bone marrow >10%
Monoclonal antibody in serum/ urine
\+ 1 of CRAB:
Hypercalcaemia
Renal failure
Anaemia
Lytic bone lesions
89
Q

What causes malaria infection?

A

Plasmodium species

90
Q

Give the 5 species of plasmodium

A 
P. falciparum
P. vivax
P. malariae
P. ovale
P. knowlesi
91
Q

Which are the two main cell types affected by malaria?

A

Hepatocytes and RBCs

92
Q

How does sickle cell anaemia protect against plasmodium vivax?

A

P. vivax targets the Duffy antigen, sickle RBCs have no Duffy antigen

93
Q

Which other diseases provide protection against malaria and how do they do this?

A

Thalassemia and G6PD deficiency make parasite-infected erythrocytes more susceptible to dying from oxidative stress

94
Q

What is the mosquito responsible for carrying malaria?

A

Female Anopheles mosquito

95
Q

How does the plasmodium species enter the host?

A

Sporozoites in the mosquito’s salivary gland spill into the blood stream and reach the liver

96
Q

What type of reproduction occurs in the liver when the plasmodium sporozoites enter in malaria?

A

Asexual

97
Q

Which strains of malaria invade RBCs of all ages?

A

P. ovale and P. falciparum

98
Q

Which strain of malaria invade reticulocytes?

A

P. vivax

99
Q

Briefly describe the erythrocytic phase of malaria

A

Early trophozoite develops and multiplies within RBC, this ruptures and new merozoites go on the invade new RBCs

100
Q

What would occur next if a merozoite undergoes gametogony?

A

Gametocytes remain inside RBC and may be taken up by a female Anopheles mosquito
Gametocytes reach the mosquito’s gut and mature/ fuse into zygote
Oocyst ruptures releasing sporozoites

101
Q

Give 4 symptoms of haemolytic anaemia secondary to malaria

A

Extreme fatigue
Headaches
Jaundice
Splenomegaly

102
Q

Why do you get paroxysms of fever in malaria?

A

The release of TNF-alpha and other inflammatory cytokines correspond to the rupture of infected RBCs
Paroxysms vary depending on the length of the erythrocytic phase

103
Q

Where are most plasmodium-infected RBCs destroyed?

A

Sleen

104
Q

How does P. falciparum avoid destruction by the spleen and cause ischaemic damage?

A

It generates a sticky protein that coats the surface of the infected RBCs
This protein causes RBCs to clump together and jam up blood vessels
Cytoadherence means infected cells can’t flow to the spleen
It also blocks blood flow to vital organs

105
Q

Give 3 symptoms of cerebral malaria

A

Altered mental status
Seizures
Coma

106
Q

Give 4 symptoms of bilicus malaria

A

Diarrhoea
Vomiting
Jaundice
Liver failure

107
Q

How would you diagnose malaria?

A

Thick blood smear: locates parasites in RBCs
Thin blood smear: directly identifies plasmodium species
>5% of parasitemia can have worse outcomes
Thrombocytopenia
Elevated lactate dehydrogenase due to haemolysis
Normochromic and normocytic anaemia

108
Q

Give the 4 general types of treatment for malaria

A

Suppressive treatment/ chemoprophylaxis
Therapeutic treatment
Gametocidal treatment
Radical treatment

109
Q

Explain the difference between the three types of recurrent malaria

A

Recrudescence- from infective treatment that did not clear the infection, common with increase in antimalarial resistance
Relapse- blood cleared of merozoites but hyptozoites persist in the liver
Reinfection- treated but a new infection causes a new bout of malaria

110
Q

Give 4 means of preventing malaria

A

Mosquito nets
Full body clothing
Indoor insecticide sprays
Empty stagnant collections of water

111
Q

Define polycythaemia

A

Elevated haematocrit (% of RBCs in the blood)

112
Q

Describe the difference between absolute and relative polycythaemia

A

Absolute is an increase in RBCs

Relative is due to a decrease in plasma volume

113
Q

Give 4 causes of absolute polycythemia

A

Myeloproliferative syndrome
Reaction to chronically low oxygen levels
Malignancy
Being over-transfused

114
Q

Give 3 causes of relative polycythemia

A

Burns
Dehydration
Stress

115
Q

Give 4 causes of an increase in procoagulants

A 
Sepsis
Malignancy
Trauma
Obstetric complications
Intravascular haemolysis
116
Q

Give 3 examples of procoagulants

A

Tissue factor
Lipopolysaccharide
Enzymes that activate clotting factors

117
Q

Give 3 consequences of new clot formation

A

Ischameia
Depletion of platelets and clotting factors
Fibrin degradation products in circulation interferes with clot formation

118
Q

What would be the lab findings with disseminated intravascular coagulation?

A

Decrease in platelets and fibrinogen
Prolonged prothrombin and partial thromboplastin time (PT and PTT)
Increase in D-Dimers

119
Q

What might the lab findings be in a patient with chronic DIC?

A

Normal results due to compensation

Medicine Phase 2A (OWN) (10 decks)

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