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2b deck > Haem important > Flashcards

Haem important Flashcards

1
Q

what cells are affected in Multiple myeloma? what is the effect?

A

Abnormal plasma cells (antibody-producing B lymphocytes) accumulate in the bone marrow and replicate in an uncontrolled way –> leads to one specific type of immunoglobulin being massively overproduced.

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2
Q

presentation of multiple myeloma

A
  • CRABBI: hyperCalcaemia, Renal failure, Anaemia, Bone lesions (and bone pain), Bleeding, Infection
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3
Q

multiple myeloma investigations

A
  • Bloods: FBC- anaemia and thrombocytopoenia, U&Es- raised urea and creatinine + raised calcium
  • raised conc of IgA/IgG on serum/urine electrophoresis
  • Bone marrow aspiration/trephine biopsy CONFIRMS DIAGNOSIS
  • whole body MRI done to survey skeleton for bone lesions
  • Rouleaux formation on blood film
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4
Q

3 criteria for diagnosing multiple myeloma

A

1- monoclonal plasma cells in bone marrow >10%
2- monoclonal protein within serum or urine
- evidence of end-organ damage (hypercalcaemia, elevated creatinine, anaemia, lytic bone lesions/fractures)

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5
Q

treatment of myeloma

A
  • under 65: stem cell transplant + Bortezomib (chemo) + dexamethasone
  • Over 65: just chemo
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6
Q

hodgkin’s lymphoma- causes

A

mononucleosis infections from EBV or CMV

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7
Q

What cells are affected in Hodgkin’s kymphoma and what is the effect?

A

B lymphocytes stop expressing antibodies due to mutations but do not die due to mutations in the Fas gene –> they develop own self regulatory growth mechanism + become large cells (REED STERNBERG CELLS)

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8
Q

appearance of Reed-Sternberg cells on histology

A

“owl-like” (because multi-nuclei)
lunar histiocytes
giant malignant cells

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9
Q

management for Hodgkin’s

A 
ABVD chemo: 
Adriamycin 
Bleomycin 
Vinblastine 
Dacarbazine
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10
Q

is Hodgkin’s contiguous

A

yes- only spreads to ADJACENT lymph nodes/structures due to flow of lymph- doesn’t arise in several unlinked structures

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11
Q

investigations hodgkin’s

A
  • bloods: normocytic anaemia (low number RBCs), oesinophilia (abnormally high eosinophils)
  • Raised LDH (serum lactate dehydrogenase)
  • lymph node biopsy- reed sternberg cells
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12
Q

non-hodgkins’ lymphoma symptoms

A
  • Painless lymphadenopathy (non-tender, rubbery, asymmetrical)
  • Constitutional/B symptoms (fever, weight loss, night sweats, lethargy)
  • Extranodal Disease - gastric (dyspepsia, dysphagia, weight loss, abdominal pain), bone marrow (pancytopenia, bone pain), lungs, skin, central nervous system (nerve palsies)
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13
Q

differentiating between Hodgkin’s and Non-hodgkin’s lymphoma

A
  • Biopsy- Hodgkin’s contains Reed-sternberg cells
  • Hodgkin’s lymphadenopathy triggered by alcohol
  • B symptoms typically occur earlier in Hodgkin’s lymphoma and later in non-Hodgkin’s lymphoma
  • Extra-nodal disease is much more common in non-Hodgkin’s lymphoma than in Hodgkin’s lymphoma
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14
Q

2 examples of non-hodgkin’s lymphoma

A

MALT (mucosa associated lymphoid tissue)- occurs normally in stomach, often associated with H pylori infection

Burkitt’s lymphoma; associated with west africa, childhood disease, jaw lymphadenopathy - often associated with malaria infection

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15
Q

Investigations for non-hodgkin’s

A
  • excisional node biopsy= diagnostic
  • CT chest/abdo/pelvis for staging
  • HIV test (HIV= risk factor for NHL)
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16
Q

staging system for lymphoma

A 
Ann-Arbor: 
•I: single lymph node
•II: 2 or more lymph nodes/regions on same side of diaphragm
•III: nodes on both sides of diaphragm
•IV: spread beyond lymph nodes
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17
Q

Treatment for high-grade non-hodgkin’s

A

RCHOP

  • Rituximab
  • Cyclophosphamide
  • Hydroxyduanomycin
  • Oncovin
  • Prednisolone
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18
Q

treatment for low grade non-hodgkin’s

A

chlorambucil for chemo, a-interferon/rituximab to maintain remission

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19
Q

what type of cells does leukaemia affect?

A

Blast cells- white blood cells which are not developed

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20
Q

what are the two types of acute leukaemia?

A

1- ALL- acute lymphoblastic leukaemia- too many lymphoblasts in the blood and bone marrow. Most common malignancy in childhood
2- AML- acute myeloid leukaemia- too many myeloblasts in blood and bone marrow (immature WBCs which become neutophils/eosinophils/basophils)

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21
Q

what % of bone marrow is blast cells in acute leukaemia? what is the effect?

A

more than 20% (normally should be 1-2%)
large proportion of blast cells means other cells cant differentiate or be produced in bone marrow properly –> leads to anaemia (fatigue), thrombocytopoenia (bleeding), neutropoenia (infection)

22
Q

symptoms of acute leukaemia

A
  • bone marrow failure- anaemia (tiredness, SOB, weakness), thrombocytopenia (bleeding + bruising), Leukopenia (infection), bone marrow infiltration (bone pain)

systemic signs- fever, pallor, petechiae

ALL: lymphadenopathy, hepatosplenomegaly, testicular enlargement

AML: violaceous skin lesions

23
Q

investigations acute leukaemia

A
  • FBC- low Hb, high WBC, low platelets
  • blood film shows blast cells, in ALL large blast cells, in AML there are AUER RODS
  • CXR shows mediastinal widening in T-cell ALL
24
Q

treatment in acute leukaemia

A

1 - remission induction- chemo destroys majority of tumour
2- remission consolidation- involves bone marrow transplant
3- maintainign remission + supportive care

25
Q

distinguishing between chronic and acute leukaemia

A

in chronic, blast cells mature partially whereas in acute, they don’t mature at all

26
Q

philadelphia chromosome

A

chromosome abnormality seen in CHRONIC MYELOID LEUKAEMIA

27
Q

most common of all leukaemias

A

chronic lymphoid leukaemia

28
Q

treatment of CML

A
  • biological therapy- tyrosine kinase inhibitor (e.g. Imantinib), prevents action of Philadephia chromosome
  • chemo
  • stem cell transplant
  • bone marrow transplant
29
Q

risk factors for CLL

A

low immunity due to HIV/AIDS

30
Q

which cancer is also known as lymphocytic lymphoma

A

mature CLL (because leads to formation of masses in lymph nodes)

31
Q

smudge cells are seen on the blood film in

A

chronic lymphocytic leukaemia

32
Q

which cells are affected in CML v CLL

A

CML- affects basophils, neutrophils and eosinophils (granulocytes)
CLL- affects B lymphocytes

33
Q

treatment of CLL

A

1st line: fludarabine, cyclophosphamide or rituximab

2nd line: chlorambucil with prednisolone

34
Q

what is microcytic anaemia? what are the causes?

A

Small RBCs in peripheral blood smear, usually characterised by low MCV
Causes= TAILS:
- Thalassaemia
- Anaemia of chronic disease (can occur with illnesses like TB, Crohns, RA, lupus, polymyalgia etc)
- Iron deficiency
- Lead poisoning
- Sideroblastic anaemia (bone marrow produces ringed sideroblasts instead of healthy RBCs)

35
Q

Normocytic anaemia- what is it? what are the causes?

A

normal MCV and normal haem levels, but insufficient numbers of RBCs
caused by
- Haematological disorders such as aplastic anaemia and some haemolytic anaemias
- Anaemia of chronic disease
- Acute blood loss
- Endocrine disorders
- Combined haematinic deficiency (iron, B12 AND folate deficiency)

36
Q

Macrocytic anaemia- what is it and what are the causes

A

RBCs are larger than their normal volume (high MCV)

causes:
- B12/folate deficiency
- Alcohol excess/liver disease
- Hypothyroid disease
- Haematological causes; antimetabolite therapy, haemolysis, bone marrow failure and bone marrow infiltration

37
Q

What is Polycythaemia rubra vera? what mutation is present in over 90% of cases?

A

-a myeloproliferative disorder where too many
RBCs are produced by the bone marrow. Primary cause of polycythaemia (high concentration of RBCs in the blood)
- JAK2 mutation in haemopoietic myeloid stem cells–> no apoptosis –> proliferation of RBCs, WBCs and platelets
- can lead to hyper-viscosity and thrombosis

38
Q

presentation of polycythaemia rubra vera

A

Characteristic signs : itch after hot bath &
erythromelalgia (burning sensation in fingers +
toes)
• Hyper viscosity can cause headaches, dizziness,
tinnitus, visual disturbance
• Facial plethora + splenomegaly on examination
• Gout (due to high urate from RBC turnover)
• Features of arterial or venous thrombosis may be
present

39
Q

Investigations for polycythaemia rubra vera

A
  • RAISED RED CELL MASS ON CHROMIUM STUDIES AND SPLENOMEGALY
  • FBC: high red cell count, high Hb, high haematocrit, high packed cell volume and sometimes high WBC count and platelets
  • increased B12
  • Marrow shows hypercellularity with erythoid hyperplasia
40
Q

treatment for polycythaemia rubra vera

A
  • aim to keep haematocrit below 0.45 to reduce risk of thrombosis
  • venesection (young low risk pts)
  • hydroxycarbamide (hydroxyurea) if old or previous thrombosis
  • a-interferon for women of childbearing age
41
Q

sickle cell anaemia pathology

A

mutation in the HBB gene causes the Beta globin chains in Haemoglobin A to be misshapen (mutation causes amino acid substitution in gene coding the Beta globin chain, causing production of HbS instead of HbA)
- HbS polymerises when deoxygenated, causing RBCs to deform, producing sickle cells- these are fragile, haemolyse and block small blood vessels
- Sickling happens a lot when theres acidosis
because Hb’s affinity for oxygen decreases & in
low flow blood vessels because Hb has lots of time
to dump O2 = the Hb is deoxygenated so the RBC
sickles
- Repeated sickling of RBCs damages the RBCs cell
membrane which leads to premature destruction
- called intravascular hemolysis. This causes
anaemia + spillage of Hb into vessels that joins
with haptoglobin to be recycled (hence low
haptoglobin)

42
Q

inheritance pattern sickle cell

A

autosomal recessive

43
Q

investigations- sickle cell

A
  • protein electrophoresis of Hb to find HbS
  • blood smear shows sickled cells
  • can be diagnosed at birth using newborn blood spot screen using cord blood
44
Q

symptoms sickle cell

A
  • anaemia , enlarged cheeks, hair on end appearance on skull
  • hepatomegaly
  • jaundice, bilirubin gallstones
  • pain and avascular necrosis (due to vaso-occlusion through sickled cells getting stuck)
45
Q

treatment of sickle cell
1- long term management
2- crisis management

A

1- hydroxycarbamide

2- analgesia (opiates), rehydration, oxygen, antibiotics if evidence of infection, blood transfusion

46
Q

Von Willebrand disease signs, investigations, treatment

A

signs- bruising, epistaxis, menorrhagia, increased bleeding post tooth extraction
- Investigations: increased activated partial thromboplastin time, increased bleeding time
Treatment: desmopressin used in
mild bleeding, WVF-containing factor VIII
concentrate for surgery/major bleeds, avoid NSAIDs

47
Q

Thrombocytic thrombocytopenic purpura (TTP) - signs and treatment

A

TPP pentad: Microangiopathic haemolytic anaemia, Thrombocytopenic purpura, neurological abnormalities, fever, renal disease

treatment: emergency- urgent plasma exchange, steroids, eculizumab (mab)

48
Q

4 organisms which cause malaria + which is most deadly?

A

plasmodium falciparum/vivax/ovale/malariae, plasmodium falciparum is most deadly , vivax is most likely non-deadly cause

49
Q

treatment for malaria

A

Artesunate (severe or uncomplicated) - quinine is second line if artesunate is unavailable
Chloroquine

50
Q

Sepsis 6

A
  1. give high flow oxygen
  2. Blood cultures
  3. Antibiotics within first hour
  4. give fluid challenge
  5. measure lactate
  6. measure urine output

2b deck (18 decks)

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