Haematology & Immunology Flashcards
(98 cards)
1
Q
What are the main features of myeloma? (CRAB)
A
→ HyperCalcaemia
→ Renal failure
→ Anaemia
→ Bone disease
2
Q
What is lactate a marker of?
Is a high or low lactate good?
A
Hypoperfusion (reduced O2 reaching the tissues)
LOW lactate - the higher the lactate, the more tissues are without O2!
3
Q
What is the function of haptoglobin?
A
It transports free haemoglobin in the bood → reticuloendothelial system to be recycled
4
Q
Which ethnic group is sepsis most common within?
A
Asians
5
Q
What is a characteristic finding on a blood film that indicates Hodgkins lymphoma?
A
Reed-sternberg cells
6
Q
List 4 risk factors for Hodkins lymphoma:
What is the key presenting symptom?
What is the diagnostic test/ investigation?
~ What is a key finding in this?
What is the staging used in all lymphoma’s? - describe the stages
A
→ Smoking
→ Epstein barr virus
→ HIV
→ Immunosuppression
Lymphadenopathy - non-tender, alcohol causes pain in lymph nodes
Lymph node biopsy
~ Reed sternberg cells
Ann Arbor Staging:
Stage 1: Only 1 lymph node group affected
Stage 2: Several lymph nodes affected but on the same side of diaphragm
Stage 3: Several lymph nodes affected but on different sides of diaphragm
Stage 4: Organ invovlement (eg, lungs/ liver)
7
Q
What is the name given for premature RBCs? (these are the RBCs just before they are released into the circulaton)
A
Reticulocytes
8
Q
What is the difference between petechiae & purpura?
What is ecchymoses?
A
- *Petechiae** < 3mm
- *Purpura** 4 - 10mm
Ecchymoses is bleeding under the skin that is larger than 1cm!
9
Q
In haemotology, what is the function of G6PD?
What is the result of a G6PD deficiency?
List some common triggers of this: (3)
What ar the common clinical features seen? (3)
A
G6PD is an enzyme that attaches onto RBCs to protect them against oxidative stress
G6PD deficiency causes haemolysis of RBC when there is oxidative stress → haemolytic anaemia
1) Infection
2) Broad beans (fava beans)
3) Drugs (antimalarials, nitrofurantoin, aspirin)
1) Anaemia
2) Jaundice
3) Splenomegaly
10
Q
Anaphylaxis is what type of hypersensitivity reaction?
This type of reaction is mediated by what?
A
Type 1 hypersensitivity reaction
IgE mediated mast cell degranulation
11
Q
What is Immune Thrombocytopenic Purpura (ITP)?
What blood abnormality does it result in?
What is the 1st line treatment for ITP?
If this doesn’t work, what do you add to the treatment?
A
Autoimmune attack of platelets (antibodies are made against platelets)
Results in thrombocytopenia (low platelet count)
1st line treatment: steroids
If steroids don’t work, add in IV IgG (immunoglobulins)
12
Q
What blood levels of Hb would indicate anaemia in:
- a -* females
- b -* males
A
Females: < 120 g/L
Males: < 140 g/L
13
Q
What is a characteristic finding on a blood film that indicates acute myeloid leukamia?
A
Auer rods
14
Q
What system is used to stage lymphoma’s?
A
Ann Arbor staging
15
Q
Cancers within the bone marrow can cause what result on a FBC?
Why can this occur?
A
Pancytopenia
Occurs when the cancerous occupy most of the space within the bone marrow - normal blood cells are unable to develop!
16
Q
Give the medical name for a red blood cell.
What is the name given to the production of RBCs?
What hormone is responsible for stimulation of RBC production?
Where is this hormone secreted from & why is it secreted?
A
Erythrocyte
Erythropoesis
Erythropoietin
Kidney in response to hypoxia
17
Q
What are the 2 antibiotics that are started if neutropenic sepsis is suspected?
A
~ Tazocin
~ Gentamicin
18
Q
What immunological mechanism is responsible for type 2 hypersensitivity reactions?
A
Auto-antibody mediated receptor activation
19
Q
What is the qSOFA score used for?
What 3 variables does the qSOFA consider?
A score of what suggests a poor prognosis?
A
Used on patients with a suspected/ confirmed infection to predict the patients who would likely require a higher level of care & have a poorer prognosis
→ BP
→ Mental state (level of conscousness)
→ Respiratory rate
Score of 2 or more
20
Q
What is the prophylaxis management of haemophilia?
How is an acute episode of bleeding treated? (3)
A
Replacement of clotting factors via IV transfusions (VIII - A, IX - B)
1) Infusions of affected clotting factor (VIII or IX)
2) Desmopressin (DDAVP) - to stimulate VWF release
3) Tranexamic acid - reduces the rate of fibrinolysis so that clot remains for longer
21
Q
List some causes for a decreased production of RBC’s in the bone marrow (4)
A
Bone marrow disorder
Chronic kidney disease (reduced secretion of erthyropoietin reduces RBC production!)
Hypothyroidism (thyroid hormones also stimulate RBC production)
Iron & vitamin B12 deficiency (these are needed for functional RBC production)
22
Q
What is the abnormality that results in polycythaemia vera?
What mutation is associated with polycythaemia vera?
List some clinical signs/ symptoms of this condition: (5)
What is the management of this condition?
A
Proliferation of RBC’s
JAK2 mutation
- Red face (plethora)
- Vascular occlusion (DVT/ PE/ Stroke)
- Splenomegaly
- Headaches
- Itchy, especially after hot bath
Management: venesection (to prevent hyperviscosity of blood) & aspirin
23
Q
Name the 2 divisions of the immune system:
A
Innate & adaptive immune systems
24
Q
Regarding fluids, (colloid & crystalloid’s):
1) give an example of each type commonly used in hospital
2) describe the size of the molecules they contain & the consequence of this on fluid compartments within the body
3) state a contraindiction in each type
A
- *1) Colloid**: fluid containing starch/ gelatin
- *Crystalloid**: plasmalyte/ hartmans/ dextrose/ 0.9%NaCl
- *2) Colloid:** large molecules → more fluid is retained in the blood vessels
- *Crystalloid:** small molecules → some fluid remains in blood vessels & some moves into the tissues/ cells
- *3)** Colloid: the large molecules can cause kidney damage (so cannot be used in patients with renal failure)
- *Crystalloid:** 0.9%NaCl has a high Na conc so can cause hypernatraemia
25
What is lactate a marker of?
Is a high or low lactate good?
Hypoperfusion (reduced O2 reaching the tissues)
LOW lactate - the higher the lactate, the more tissues are without O2!
26
What abnormality is seen in haemophilia A?
What abnormality is seen in haemophilia B?
What is the mode of inheritance of haemophilia?
What tests would you do to diagnose haemophilia and what results would you expect in haemophilia? (3)
Haemophilia A: deficiency of clotting factor VIII
Haemophilia B: deficiency of clotting factor IX
X linked recessive
1) Clotting factor tests - to look at levels of factors VIII & IX (low VIII in haemophila A & low IX in haemophilia B)
2) Blood test- APTT\*: prolonged
3) Blood test- prothrombin: normal
\* APTT = blood test that measures time taken for blood to clot
27
Which electrolyte abnormality can blood transfusions cause?
Why does this happen?
Hypocalcaemia
When blood is donated, it's mixed with **sodium citrate** to prevent it from coagulating. → The citrate in the blood can bind to the patient's circulating calcium resulting in a decreased amount of free calcium = symptoms of hypocalcaemia
28
What test would be used to test for an autoimmune cause of haemolytic anaemia?
What result would suggest an autoimmune cause & what would be seen in the lab?
DAT test (direct antiglobulin test) / coombs test (old name)
Positive result = immune mediated
Agglutination of RBCs (they clunp together)
29
List some common presentations of von Willebrand disease: (5)
→ nose bleeds
→ menorrhagia
→ bleeding gums when brushing teeth
→ prolonged, heavy bleeding during surgery/ trauma
→ easy bruising
30
What is the normal range of WBC in blood?
4 - 10 x109/L
31
What are 3 commonest pathogens responsible for causing neonatal sepsis?
What antibiotics are used in the 1st line management of neonatal sepsis?
1) Group-B strep
2) E.Coli
3) Listeria
IV penicillin & gentamicin
32
What is the function of Von Willebrand Factor?
What abnormality results in von Willebrand disease?
What is the mode of inheritance of VWD?
VWF is vital for clot formation: • links platelets to the exposed, damaged vessel wall • stabilises factor VIII so that it can work for longer
A deficiency of, or dysfunctional VWF
Autosomal dominant
33
What is the treatment of von Willebrand disease?
List 2 contraindictations to the use of DDAVP:
There is no day-to-day treatment. Treatment is given after a bleed or in preparation for surgery
1) VWF concentrate IV
2) Desmopressin - stimulates the release of VWF
3) Tranexamic acid - inhibits fibrinolysis (clot breakdown)
Contraindictations: young children, people with high cardiovascular risk
34
What is an autologous transplant?
What is an allogeneic transplant?
What is a syngeneic transplant?
What is an xenogeneic transplant?
What type of transplant has the highest risk of rejection?
**Autologous transplant:** tissue from the same person
**Allogeneic transplant:** tissue from another member of the same species (eg, human - human)
**Syngeneic transplant:** tissue from an identical twin
**Xenogeneic transplant:** tissue from a different species
Xeogeneic transplant has the biggest risk of rejection as it is tissue from another species
35
What is the cellular pathology that results in pernicious anaemia?
Autoimmune attack against intrinsic factor → B12 cannot be absorbed without intrinsic factor and patient becomes anaemic
36
What is a **characteristic** finding on a **blood film** that indicates **chronic lymphocytic leukaemia**?
**Smudge** cells
37
Skin prick testing is used to test for what type of hypersensitivity reaction?
Patch testing is used to test for what type of hypersensitivity reaction?
**Skin prick testing** = hypersensitivity I
**Patch testing** = hypersensitivity IV
38
What is the function of haptoglobins?
They remove free haemoglobin from the circulation
39
What chromosome is associated with chronic myeloid leukaemia? - what are the consequences of this?
What is the gene translocation?
What is the 1st line management of CML?
**Philadelphia chromosome** ⇒ BCR-ABL gene (oncogene)
**t (9;22)**
Tyrosine kinase inhibitors (inhibit BCR-ABL!)
~ eg **Imatinib**
40
What is the difference between Hodgkins and Non-Hodgkins lymphoma?
Hodgkins lymphoma is characterised by the presence of Reed-Sternberg cells → Non-Hodgkins lymphoma does *not* have these cells.
\* Reed-Sternberg cells are abnormally large lymphocytes that usually have multiple nuclei
41
What immunological mechanism is responsible for type 2 hypersensitivity reactions?
Give 2 examples of conditions that this occurs in:
Auto-antibody mediated receptor activation
Haemolytic disease of the newborn
Transfusion reactions
42
You are working in A&E and a patient is hypotensive. What do you do to increase the BP?
How much of this would you give and over what time?
IV fluid resuscitation
500ml saline or plasmalyte bolus over 15 mins
43
What is a type 4 hypersensitivity reaction?
Give 2 examples of conditions that are caused by type 4 hypersensitivity reactions:
Delayed hypersensitivity reaction, mediated by T cells
**Autoimmune conditions:**
Rheumatoid arthritis
Type 1 Diabetes
44
What are the cancerous cells in myeloma & what do they produce? - explain what these are..
List some signs/ symptoms of myeloma: (4)
Name the definitive investigation of myeloma:
What would be seen on a bone marrow biopsy? - state what would qualify as myeloma
Plasma cells - produce paraproteins
**Paraproteins =** identical immunoglobulins (usually IgG) produced by a (*cancerous)* clonal population of plasma cells
* Hypercalcaemia
* Renal failure
* Anaemia
* Lytic bone disease/ pain
**Serum protein electrophoresis**
Bone marrow biopsy: high plasma cells
~ plasma cells \>10% = myeloma
~ plasma cells 3-10% = MGUS
45
What is graft vs host disease?
How can the risk of GVHD be minimised?
Rejection of a transplant caused by the **donor's** T cells attacking the **recipant's** antigens !!
**Immunosuppression!**
• steroids
• cyclosporin/ rapamycin
46
In haematology, what 3 things are considered as 'B symptoms'?
Night sweats, weight loss, fever
47
What is the commonest blood cancer of children?
What blood cell line does this cancer arise from?
List some symptoms/ signs of this cancer: (4)
What is the definitive investigation? What will be seen on this?
What is the treatment of this cancer?
**Acute lymphoblastic leukaemia**
Lymphoid progenitor cells (undifferentiated)
* Child with a limp
* Bone/ joint pain
* Exertional SOB
* Pancytopenia
Bone marrow biopsy - *blast cells*
Prolonged course of chemotherapy
48
What cells are cancerous in **acute myeloid leukaemia**? - where in the body are these cancerous cells found? *(before mets)*
List some clinical signs/ symptoms of AML: (4)
What is the definitive investigation of AML?
~ List 2 things that would be seen on this
What is the treatment of AML?
Undifferentiated, myeloid progenitor cells
~ found in the bone marrow
* Pancytopenia
* Gum hypertrophy
* Hepatosplenomegaly
* Petechiae & abnormal bleeding (caused by low platelets)
**Bone marrow biopsy**
• \> 20% blast cells
• auer rods
Chemotherapy +/- stem cell transplant
49
Name the 2 types of lymphocytes and name where they each mature
T cells - thymus
B cells - bone marrow
50
Why does physiological anaemia occur during pregnancy?
Blood volume increases during pregnancy, but plasma volume \> RBC = anaemia (as RBC's are diluted!)
51
Which compound is released from damaged vessel walls and initiates the coagulation cascade?
Tissue factor
52
What does SIRS stand for?
What clinical features would a patient have, to be diagnosed with SIRS?
Systemic inflammatory response syndrome
→ High/low temperature
→ HR \> 90
→ RR \> 20
→ High CO2
→ High WBC's
53
Give examples of conditions that cause a normocytic anaemia: (4)
What initial investigation would you do after identifying normocytic anaemia & what would high / low results suggest?
1) Blood loss
2) Haemolysis of RBC (aka, haemolytic anaemia)
3) Bone marrow disease (failure/ cancer infiltration)
4) Secondary anaemia (eg, inflammation)
***Reticulocyte count:***
High reticulocyte = Blood loss, haemolysis
Low reticulocyte = Bone marrow disease, secondary anaemia
54
What is the medical word for a high platelet count?
What is the medical word for a low platelet count?
Thrombocytosis
Thrombocytopenia
55
What immunological mechanism is responsible for type 3 hypersensitivity reactions?
Give an example of a disease that is caused by type 3 hypersensitivity.
Immune complex deposition
SLE
56
What are the main features of myeloma? (CRAB)
→ Hyper**_C_**alcaemia
→ **_R_**enal failure
→ **_A_**naemia
→ **_B_**one disease
57
What does SCID stand for?
Which immune cells are affected in SCID?
What are the 2 treatment options for SCID?
Severe combined immunodeficiency
Development of B cells & T cells is affected producing dysfunctional B & T cells
1st line = stem cell transplant
If not available: gene therapy
58
List some common symptoms of anaemia: (5)
→ Fatigue
→ SOB
→ Headaches
→ Pre-syncope / syncope
→ Palpitations
59
What is the prophylaxis management of haemophilia?
How is an acute episode of bleeding treated? (3)
Replacement of clotting factors via IV transfusions (VIII - A, IX - B)
1) Infusions of affected clotting factor (VIII or IX)
2) Desmopressin (DDAVP) - to stimulate VWF release
3) Tranexamic acid - reduces the rate of fibrinolysis so that clot remains for longer
60
Name the 3 hormones that stimulate RBC production in the bone marrow:
Erythropoietin
Thyroid hormone
Androgens
61
List some clinical features seen in haemophilia: (5)
Haemarthrosis (bleeding into the joints)
Muscle haematoma
CNS bleeding
Prolonged bleeding after surgery/ trauma
Menorrhagia
62
The Philadelphia chromosome is associated with what haematological condition?
The philadelphia chromosome (a mix of 2 chromosomes) results in what oncogenic gene?
Chronic myeloid leukaemia
BCR-ABL gene
63
What type of anaemia does **sickle cell disease** cause?
Would you expect a high or low reticulocyte count? - why?
**Normocytic** anaemia (normal MCV (RBC size))
**Raised** reticulocyte count
~ there is increased haemolysis of RBC and thus the bone marrow chucks out more reticulocytes to try to compensate in the loss of RBC *(although it doesn't work as reticulocytes are immature RBC!)*
64
There are 3 types of von Willebrand Disease, describe the problem associated with each type:
Which type(s) presents with the most severe symptoms?
Type 1: there isn't enough VWF in the body
Type 2: there is enough VWF, however it is dysfunctional
Type 3: almost complete deficiency of VWF
Types 2 & 3 are more severe
65
What cells are cancerous in **myeloproliferative disorders**? - where in the body are these cancerous cells found? (*before mets)*
List some clinical signs/ symptoms of **chronic myeloid leukaemia** (a myeloproliferative disorder) (4) - what is the cancerous cell?
What chromosome is associated with CML? - what are the consequences of this?
What is the 1st line management of CML?
Differentiated cells of myeloid origin
~ found in bone marrow
• Anaemia (→ pancytopenia)
• *Massive* splenomegaly
• HIGH WCC
• Gout
~ Cancerous cell = neutrophils
**Philadelphia chromosome** ⇒ BCR-ABL gene (oncogene)
Tyrosine kinase inhibitors (inhibit BCR-ABL!)
66
What are the 6 components of sepsis 6?
~ state the order you would do these in
(take 3, give 3)
1) Give O2 if sats are below 94%
2) Take blood cultures
3) Give IV antibiotics
4) Fluid challenge (give IV fluids)
5) Measure blood lactate
6) Measure urine output
67
What are the 6 components of sepsis 6?
~ state the order you would do these in
(take 3, give 3)
**1)** Give O2 if sats are below 94%
**2)** Take blood cultures
**3)** Give IV antibiotics
**4)** Fluid challenge (give IV fluids)
**5)** Measure blood lactate
**6)** Measure urine output
68
What does thrombocytopenia mean?
List some common presentations of thrombocytopenia: (5)
Low platelet count
→ Petechiae
→ Ecchymosis (bruising)
→ Nose bleeds
→ Bleeding gums
→ Menorrhagia
69
What condition is indicated if a woman presents with **recurrent miscarriages** & a history of **VTE** events?
What is the treatment of this condition? (2)
**Antiphospholipid syndrome**
Aspirin & LMWH
70
SIRS + infection = ?
What is the condition called if a patient has end organ damage as a result of sepsis?
What is the difference between severe sepsis & septic shock?
Sepsis
Severe sepsis
In septic shock, the patient has ***hypotension*** as well as severe sepsis
71
A 16y boy presents with central abdominal pain & haematuria for 1 week. He also complains of pain in both knees. Examination reveals a non-blanching purpuric rash on his legs & buttocks. Urine dip shows blood ++ & protein +, kidney function is abnormal.
What is the most likely diagnosis? - what is this?
List the 4 common presenting features of this condition:
What is the management of this condition?
What monitoring needs to be done? (2)
**Henoch-Schonlein Purpura** - A type of IgA vasculitis
* Purpura (rash on legs → buttocks)
* Joint pain (commonly knee's & ankles)
* Abdominal pain
* Renal impairment
**Management:** supportive (analgesia, rest, hydration)
~ most usually resolve within 4-6 weeks.
**Monitoring**: needed whilst the disease is still active:
• urine dipstick (to monitor renal impairment)
• blood pressure (to monitor for hypertension)
72
What is a **characteristic** finding on a **blood film** that indicates **multiple myeloma**?
**Rouleaux formation**
73
List some causes of intravascular haemolysis: (3)
List some causes of extravascular haemolysis: (4)
**Intravascular:**
→ Mechanical heart valve
→ Acute transfusion reaction (if blood transfused is mis-matched)
→ Infections, eg malaria
→ G6PD deficiency
→ Autoimmune haemolytic anaemia
**Extravascular:**
→ Hypersplenism (spleen works harder than normal)
→ Haemoglobinopathys (eg thalassaemia, sickle cell)
74
Name the 2 ways that anaemia can be categorised by:
1. Looking at the mean corpuscular volume (MCV) of the RBCs
2. The mechanism of cause of anaemia
| (RBC size!)
75
What genetic mode of inheritance is seen in haemophilia A & B?
Which sex is haemophilia more common in?
X linked recessive inheritance!
Males
76
What does SCID stand for?
Which immune cells are affected in SCID?
What are the 2 treatment options for SCID?
Severe combined immunodeficiency
Development of B cells & T cells is affected producing dysfunctional B & T cells
1st line = stem cell transplant
If not available: gene therapy
77
In a centrifuge, what 3 components will blood separate into?
Name some cells that will be found in each component.
**_Plasma_**
→ Clotting factors
→ Albumin (& other proteins)
→ Antibodies
**_Buffy coat_**
→ Platelets
→ WBC's (leucocytes)
**_Red blood cells_**
78
What are hypersensitivity reactions?
Exaggerated immune responses that cause damage to tissues/ blood
79
If a woman is \*Rh- and is carrying a Rh+ baby and there is no intervention, what will happen during delivery/ when there is mixing of blood?
Why does this happen?
When should this be checked for during pregnancy?
What can be given as prophylaxis for this?
\*Rh = rhesus
The women will start developing anti-D antibodies after any sensitising event (commonly giving birth)
If someone is rhesus negative, they don't have the D antigen on their RBC's so if their blood comes into contact with someone that is rhesus positive then their blood will start producing antibodies against the foreign antigens.
Rh status of mother & baby is checked at the booking appointment (week 10)
If mother is negative & baby is positive, prophylaxis = anti D injection at 28 weeks gestation PLUS immediately after any sensitising events
80
What is the definition of sepsis?
Life threatening organ dysfunction caused by a dysregulated host response to an infection
81
What is the treatment of von Willebrand disease?
List 2 contraindictations to the use of DDAVP:
* There is no day-to-day treatment. Treatment is given after a bleed or in preparation for surgery*
1) VWF concentrate IV
2) Desmopressin - stimulates the release of VWF
3) Tranexamic acid - inhibits fibrinolysis (clot breakdown)
Contraindictations: youung children, people with high cardiovascular risk
82
When looking at the mean corpuscular volume of RBCs (size), what are the 3 types that may be seen?
Microcytic anaemia (small size)
Normocytic anaemia (normal size)
Macrocytic anaemia (large size)
83
If a woman is \*Rh- and is carrying a Rh+ baby and there is no intervention, what will happen during delivery/ when there is mixing of blood?
Why does this happen?
When should this be checked for during pregnancy?
What can be given as prophylaxis for this?
\*Rh = rhesus
The women will start developing anti-D antibodies after any sensitising event (commonly giving birth)
If someone is rhesus negative, they don't have the D antigen on their RBC's so if their blood comes into contact with someone that is rhesus positive then their blood will start producing antibodies against the foreign antigens.
Rh status of mother & baby is checked at the booking appointment (week 10)
If mother is negative & baby is positive, prophylaxis = anti D injection at 28 weeks gestation PLUS immediately after any sensitising events
84
There are 2 types of immunity: innate & adaptive:
1) Which one is activated in a primary/ secondary infection?
2) Which one is rapid & non-specific/ slow onset & very specific?
3) Which one provides 'short'/ 'long' term immunity?
4) Which one involves phagocytes & the complement system?
5) Which one invovles antibodies and cellular immunity (provided by T cells)?
1) **Primary** infection = innate
* *Secondary** infection = adaptive
2) **Rapid & non specific** = innate
* *Slow & very specific** = adaptive
3) **Short term immunity** = innate
* *Long term immunity** = adaptive
4) **Phagocytes & complement** = innate
5) **Antibody production & cellular immunity** = adaptive
85
What is the normal range of haemoglobin in:
1. Males
2. Females
Males: 140 - 180 g/L
Females: 120 - 160 g/L
86
Ferroportin is vital for what?
What compound blocks the action of ferroportin & what is the consequence of this?
Which organ produces this compound and in response to what 2 things?
Ferroportin is vital for **iron absorption** from gut & **iron storage** in cells, mainly liver
Hepcidin blocks ferroportin preventing further iron absorption
Liver produces hepcidin in response to:
1) high iron stores (when they are full and the body doesn't need any more iron)
2) inflammation
87
List some common signs of anaemia: (4)
→ Pallor of skin
→ Pallor of conjunctiva
→ Tachycardia
→ Raised respiratory rate
88
What is the average lifespan of a RBC?
How are RBCs removed from the circulation?
Which 2 organs are involved in this process?
120 days
The reticuloendothelial system removes RBCs from the circulation
Spleen & liver
89
What is the normal range of platelets in blood?
150 - 400 x109/L
90
What are the cancerous cells in **chronic lymphocytic leukaemia?**
List some symptoms/ signs of CLL: (4)
What autoimmune condition is associated with CLL?
What cell would be seen on a blood film?
What is the management of CLL? - is it curable?
Differentiated lymphoid cells (B & T lypmhocytes)
* COMMONLY ASYMPTOMATIC !!!!
* Non-tender lymphadenopathy
* Hepatosplenomegaly
* B symptoms
**Warm** autoimmune haemolytic anaemia
Smudge cells
NOT CURABLE - if no symptoms, don't treat!
(Otherwise chemotherapy)
91
There are 5 acute and 1 delayed complications associated with blood transfusions. **Name** each of these and **describe** the presentation/clinical features of each one:
**Anaphylactic/ allergic transfusion reaction:**
~ urticaria/ angioedema/ wheeze
~ hypotension
**Acute haemolytic transfusion reaction:**
*ABO incompatibility*
~ fever
~ hypotension
~ anxiety
~ DIC
~ jaundice
**Transfusion related acute lung injury:**
~ pulmonary oedema
~ SOB, increased RR
~ hypotension
**Transfusion associated circulatory overload:**
~ fluid overload (pulmonary oedema/ ankle oedema)
~ hypertension
**Febrile non-haemolytic transfusion reaction:**
~ fever +/- rigors/chills
\*\*\* *patients are otherwise completley FINE* \*\*\*
**Delayed haemolytic transfusion reaction:**
*Rhesus incompatibility - usually 5 days AFTER transfusion*
~ jaundice
~ anaemia
~ fever
92
A 35y/o man has been recently diagnosed with **Hodgkin's lymphoma**. He started the first day of his **chemotherapy yesterday**, but since then has **not been feeling well**. The FY2 on the ward checked his U&E and found some abnormalities including **hyperkalaemia, hyperphosphataemia and hypocalcaemia**.
What is the likely **complication** that this man has suffered from?
What can be given as **prophylaxis** against this complication?
**Tumour lysis syndrome**
Allopurinol
93
A patient had their first **chemotherapy yesterday** for an acute leukaemia and today they state that they're **not feeling very well.** This morning's bloods show **renal impairment** and a **high uric acid**.
What is the likely **diagnosis**?
**Why** does this happen?
Which **electrolyte abnormalities** would you expect to see?
**Tumour lysis syndrome**
TLS occurs due to rapid breakdown of tumour cells and thus release of intracellular contents into the blood (especially **uric acid**)
* HIGH **potassium**
* HIGH **phosphate**
* LOW **calcium**
94
Name the **commonest leukaemia in children**:
Which **genetic condition** does this leukaemia affect the most?
**Acute lymphoblastic leukaemia**
Downs syndrome
95
Name the leukaemia that can transform into a **high grade lymphoma:**
What is this transformation called?
What **diagnostic cells** would you see on a blood film in this leukaemia?
Chronic lymphocytic leukaemia
**Richter's transformation**
Smudge / smear cells
96
Which blood cancer is associated with the **Philadelphia chromosome?**
What is the translocation of this chromosome?
Chronic myeloid leukaemia
## Footnote
**t(9:22)**
97
Which **leukaemia** is often the result of the **transformation** of a **myeloproliferative disorder**?
What **diagnostic cells** would you see on a blood film in this leukaemia?
Acute myeloid leukaemia
## Footnote
**Auer rods**
98
Which 2 blood cancers would you expect to see **blast** cells in?
**ACUTE** myeloid leukaemia
**ACUTE** lymphoblastic leukaemia
