Week 9 - Haematology Flashcards
1
Q
what is the structure of erythrocytes?
A
biconcave discs = maximises surface area
anuclear
all intracellular organelles are lost in erythropoiesis
2
Q
what is the function of erythrocytes?
A
- Delivers oxygen from the lungs to the tissues all through the body
- Facilitates carbon dioxide transport
- Acts as a buffer and regulates hydrogen ion concentration
- Contributes to blood viscosity
Carries blood group antigens and Rh factor
3
Q
what types of haemoglobin are found in adults?
A
HbA
HbA2
4
Q
what is erythropoiesis?
A
process of producing RBCs
from eryhtropoietic stem cell to mature RBC
stimulated by decreased O2 in circulation which is detected by kidney which produce erythropoeitin
5
Q
what is a reticulocyte?
A
premature RBC containing ribosomal RNA
6
Q
at what point do RBCs extrude their nucleus?
A
when they’re normoblasts
7
Q
what is the function of erythropoietin?
A
regulates erythropoiesis
made in liver and kidneys
8
Q
where are most RBCs destroyed?
A
liver, spleen and lymph nodes
by macrophages
9
Q
what do RBCs break up into?
A
haem -> bilirubin
globin -> amino acids and iron
10
Q
A
11
Q
What is the main function of the spleen?
A
Filters the blood
Removes old/damaged RBCs
12
Q
What cells make platelets?
A
Megakaryocytes
13
Q
What is the main function of platelets?
A
Platelet aggregation
Plugs gap where blood clots need to form
14
Q
What is the structure of a platelet?
A
Anuclear
They are fragments of cytoplasm from megakaryocytes
Have a dense membrane and tubular network
Contain alpha bodies and dense granules
Biconvex
15
Q
What is found in the alpha granules in platelets?
A
Proteins
Factor XIII, platelet activating factor, PDGF, vWF, fibrinogen + platelet factor 4
16
Q
What is found in the dense bodies in platelets?
A
Non proteins
ADP + Ca2+ (needed for contraction and bind to vitamin K dependent factors)
17
Q
What is thrombocytopenia?
A
Not enough platelets
18
Q
What is thrombocytosis?
A
Too many platelets
19
Q
How are platelets activated? And how does aggregation occur?
A
- Platelets get exposed to endothelial damage
○ Exposed to vWF, collagen etc leads to activation- Intracellular signalling causes release of granules and generation of thromboxane
- Secondary mediators reinforce the platelets activation and activate further platelets
- Thrombin generation causes further activation of platelets
- Intracellular signalling leads to integrin activation
- Active integrin binds fibrinogen and causes platelet aggregation
- This forms the platelet aggregate primary plug
- Thrombin converts fibrinogen in the platelet aggregate to cross linked fibrin
○ This forms the secondary haemostatic plug = thrombus
20
Q
What is the structure of a neutrophil?
A
They have a characterise multilobed nucleus, with 3-5 lobes joined by slender genetic material.
21
Q
What is the function of a neutrophil?
A
First cell when body is exposed to infection and mature neutrophils (polymorphonuclear neutrophils) ingest microorganisms, help defence of body as they are actively phagocytic.
22
Q
What is the structure of eosinophils?
A
Larger cytoplasmic granules, tend not to have more than 3 lobes.
23
Q
What is the function of eosinophils?
A
Provide protection against parasite infections.
Involved in the allergic responses.
24
Q
What is the structure of a basophil?
A
Usually consist of 2 nuclear segments, cytoplasmic granules contain heparin and histamine.
25
What are found in the granules in basophils?
Heparin
Histamine
26
What is the function of basophils?
They mature in tissues to form mast cells.
Both play a role in hypersensitivity – release inflammatory molecules such as histamine to defend body from allergens, pathogens and parasites.
Basophils also release enzymes to improve blood flow and prevent blood clots.
27
What is the structure of monocytes?
Spherical cell with prominent surface ruffles and blebs
28
What is the function of monocytes?
Made in bone marrow and travels through the blood to tissues in the body where it differentiates to becomes a macrophage or a dendritic cell when body is exposed to a foreign body.
Macrophages are innate immune cells which are involved in the detection, phagocytosis and destruction of bacteria and other harmful organism.
29
What are the 3 types of lymphocytes?
T cells
B cells
NK cells
30
What is the structure of natural killer cells?
NK cells tend to be larger cells with relatively large granules scattered in their cytoplasm.
31
What is the function of T cells?
responsible for cell-mediated cytotoxic reactions and for delayed hypersensitivity responses. T lymphocytes also produce the cytokines that regulate immune responses and provide helper activity for B cells
32
What is the function of b cells?
B lymphocytes can capture, internalize, and present antigens to T cells and are the precursors of immunoglobulin-secreting plasma cells
33
What is the function of NK cells?
NK cells account for innate immunity against infectious agents and transformed cells that have altered expression of transplantation antigens
34
What is the universal blood donor? Why?
O-
Contains no clinically relevant ABO and Rh antigens
35
What antigens do each blood group have?
• Group A erythrocytes only have the A antigen
• Group B erythrocytes only have the B antigen
• Group AB erythrocytes have both the A and B antigens
• Group O erythrocytes do not have any ABO antigens
36
What antibodies do each blood group have?
• Group A individuals form anti-B antibodies
• Group B individuals form anti-A antibodies
• Group AB individuals do not form ABO antibodies
• Group O individuals form anti-A, anti-B, and anti-AB antibodies
37
What happens if a rhesus +ve mother has a rhesus +ve baby?
Do not need any additional treatment
38
What happens when a rhesus -ve mother has a rhesus +ve baby?
Baby’s blood will go into mothers system
Mothers immune system recognises rhesus D antigen as foreign and produces antibodies
The mother is then sensitised in first pregnancy
If mother becomes pregnant again with rhesus + baby then the antibodies can attack the fetus causing haemolysis
= haemolytic disease of the newborn
39
What is haemolytic disease of the newborn?
If rhesus - mother who has already had a rhesus + baby .: has developed antibodies
If have another baby that is rhesus + then mums antibodies can transfer to fetus and attack RBCs causing haemolysis
40
What is the main management of haemolytic disease of the newborn?
Prevent sensitisation
This involves giving IM anti-D injections to rhesus -ve mothers
41
What is the only antibody that can cross the placenta?
IgG
42
When are anti-D injections given?
Anti-D injections are given routinely on two occasions:
• 28 weeks gestation
• Birth (if the baby’s blood group is found to be rhesus-positive)
Anti-D injections should also be given at any time where sensitisation may occur, such as:
• Antepartum haemorrhage
• Amniocentesis procedures
• Abdominal trauma
43
what is the kleihauer test?
checks how much fetal blood has passed to the mothers during a sensitisation event
used after any sensittisation even past 20 weeks of gestation to see if another dose of antiD is required
involves adding acid to a sample of the mother’s blood.
Fetal haemoglobin is naturally more resistant to acid, so that they are protected against the acidosis that occurs around childbirth.
Therefore, fetal haemoglobin persists in response to the added acid, while the mothers haemoglobin is destroyed.
The number of cells still containing haemoglobin (the remaining fetal cells) can then be calculated.
44
what are packed RBCs?
contain erythrocytes and additives, with a negligible amount of plasma retained
only antigens need to be considered as antibodies are not present
45
what is fresh frozen plasma?
no antigens present, just red cell antibodies
46
when is fresh frozen plasma commonly used?
indicated for the deficiency of coagulation factors with abnormal coagulation tests in the presence of active bleeding.
47
what is classed as a major haemorrhage?
* Blood loss of more than one blood volume within 24 hours
* 50% of total blood volume lost in less than 3 hours
Bleeding in excess of 150 mL/minute
in acute setting:
* BP <90mmHg Systolic
HR >110bpm
48
what mnemonic is used to locate a heamorrhage?
on the floor and 4 more
- visible loss from an external wound
- Chest cavity - i.e. Haemothorax
- Abdominal Cavity - Damage to solid organ like the spleen, or damage to a major blood vessel
- Pelvis - classically from a pelvic fracture
- Long Bones - long bone fractures can account for significant blood loss
49
what are the lethal triad to avoid in major haemorrhae?
* Hypothermia: keep warm with blankets, warmed air, use a blood warmer to give blood, and when examining the patient, limit their exposure to the minimum necessary
* Acidosis: maximise oxygenation and treat/prevent hypoventilation to prevent respiratory acidosis. Avoid giving crystalloids as this can exacerbate acidosis.
* Coagulopathy: avoid crystalloids or unbalanced blood products as they can cause dilutional coagulopathy
50
in early gestation where are fetal RBCs made?
yolk sac
51
where does haematopoiesis occur from 7-15 weeks of gestation?
liver and spleen
52
when does bone marrow haematopoiesis occur in gestation?
during 3rd and 4th moth
53
what is a group and save?
samples are ABO and Rh (D) grouped and screened for atypical antibodies in the patients plasma.
kept for up to 7 days so if patient needs transfusion records are kept
54
what is done if someone urgently needs a transfusion and a group and save hasnt been done?
* 2 units of O Neg can be given if blood is required immediately
* ABO and RhD compatibility must be achieved if blood is required within 10 minutes
* A full crossmatch must be achieved if the blood is required within 20 minutes
55
what is a haemolytic transfusion reaction?
occurs when antibodies in the patient’s plasma react with antigens on transfused allogeneic red blood cells, causing haemolysis (rupture of red blood cells).
HTR occurring during or within 24 hours of transfusion is classed as acute; a delayed HTR can occur days to weeks after the transfusion.
56
what are the symptoms of a haemolytic transfusion reaction?
fever, rigors, chills, hypotension, pain, dyspnoea, tachycardia, nausea, restlessness or DIC; acute HTR can be life-threatening.
57
what is a severe allergic reaction/anaphylaxis to a transfusion?
occur when patients have immunoglobulin E (IgE) or IgG antibodies that react with proteins in transfused blood components.
58
what symptoms are seen in an allergic response to a transfusion?
become acutely dyspnoeic due to bronchospasm and laryngeal oedema and may complain of chest pain, abdominal pain and nausea.
59
what is the management of anaphylaxis to a transfusion?
* Symptoms are usually controlled by slowing the transfusion and giving antihistamine, and the transfusion may be continued if there is no progression at 30 minutes.
* Pre-treatment with chlorphenamine should be given when a patient has experienced repeated allergic reactions to transfusion.
60
what should be given before a transfusion if a patient has previously experienced repeated allergic reactions to transfusion?
chlorphenamine
61
what is given to patients at risk of iron overload in transfusions?
iron chelation therapy with desferrioxamine
62
what are the symptoms of anaemia?
* Tiredness
* Shortness of breath
* Headaches
* Dizziness
* Palpitations
Worsening of other conditions e.g. angina, heart failure, or peripheral vascular disease
63
what clinical signs are seen in anaemia?
* Pale skin
* Conjunctival pallor
* Tachycardia
Raised respiratory rate
* Koilonychia is spoon shaped nails and can indicate iron deficiency
* Angular chelitis can indicate iron deficiency
* Atrophic glossitis is a smooth tongue due to atrophy of the papillae and can indicate iron deficiency
* Brittle hair and nails can indicate iron deficiency
* Jaundice occurs in haemolytic anaemia
* Bone deformities occur in thalassaemia
Oedema, hypertension and excoriations on the skin can indicate chronic kidney disease
64
what are the causes of microcytic anaemia?
TAILS
* Thalassaemia
* Anaemia of chronic disease
* Iron deficiency anaemia
* Lead poisoning
Sideroblastic anaemia
65
patient has low serum iron, low ferritin and high total iron binding capacity. what is the cause of their anaemia?
iron deficiency anaemia
ferritin is low as all the stored iron is used up because serum iron is depleted
66
patient has low serum iron, high ferritin but low TIBC. what is the cause of their anaemia?
anaemia of chronic disease
ferritin is high due to built-up stores from hepcidin
67
patient has high serum iron, high ferritin and low TIBC. what is the cause of their anaemia?
sideroblastic anaemia
serum iron is high becuase iron builds up in cells and released into serum once the cell bursts
ferritin is high because iron overloaded state
68
what is seen on a peripheral blood film in iron deficiency anaemia?
* Cells are hypochromic (pale)
* Microcytic (small)
* Varying sizes (anisocytosis)
Abnormal shapes (poikilocytosis)
69
what is the management for iron deficiency anaemia?
* Treat underlying cause - usually involves taking iron tablets (treat the anaemia - ferrous sulphate) as well as vitamin C supplements (increase ability to absorb iron)
* Eat iron-rich food
70
what are the causes of normocytic anaemia?
either haemolysis (intravascular/extravascular) or underproduction of normal-sized RBCs
anaemia of chronic disease
comination of iron and b12/folate deficiency
71
what are the 2 types of macrocytic anaemia and what are the causes of these?
Megaloblastic anaemia - caused by impaired DNA synthesis preventing the cells from dividing properly
· B12 deficiency
· folate deficiency
Normoblastic macrocytic anaemia
· Alcohol
· Reticulocytosis (usually from haemolytic anaemia or blood loss)
· Hypothyroidism
· Liver disease
· Drugs such as azathioprine
72
what is seen on a peripheral blood film in macrocytic anaemia?
Megacities, hyper-segmented polymorphonucleated cells
(note: may be normal)
73
what is the management for anaemia from b12 deficiency?
Initially administer hydroxocobalamin 1 mg intramuscularly three times a week for 2 weeks.
The maintenance dose depends on whether the deficiency is diet related or not.
For people with B12 deficiency that is:
Not thought to be diet related — administer hydroxocobalamin 1 mg intramuscularly every 2–3 months for life.
Thought to be diet related — advise people either to take oral cyanocobalamin tablets 50–150 micrograms daily between meals, or have a twice-yearly hydroxocobalamin 1 mg injection.
Give dietary advice about foods that are a good source of vitamin B12 — good sources of vitamin B12 include:
Eggs.
Foods which have been fortified with vitamin B12 (for example some soy products, and some breakfast cereals and breads) are good alternative sources to meat, eggs, and dairy products.
Meat.
Milk and other dairy products.
Salmon and cod.
After 8 weeks of treatment, and also measure iron and folate levels.
The mean cell volume (MCV) should have normalised.
74
what is beta thalassemia cause by?
mutation on chromosome 11
causes an excess of alpha globin chains which in turn leads to cell destruction within bone, marrow and spleen.
75
what is seen on a blood film for beta thalassemia?
· Target cells, abnormal shape and size of cells:
· Hypochromia, increased polychromasia, basophilic stippling, microcytosis
76
what does G6PD deficiency cause?
haemolytic anaemia
reduced production -> rigid red cells
77
when are spherocytes seen on a peripheral blood film?
immune haemolytic anaemia
78
when are increased reticulocytes seen?
haemolytic anaemia
