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2a systems > Hematology > Flashcards

Hematology Flashcards

1
Q

what is a malignancy affecting the differentiated b cells in the bone marrow (plasma cells)

A

myeloma

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2
Q

what is a multiple myeloma

A

neoplastic monoclonal proliferation of plasma cell
myeloma affects multiple bone marrow areas in the body

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3
Q

in what condition do you find bence jones protein in urine

A

myeloma

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4
Q

pathophysiology of myeloma

A

clonal proliferation of plasma cells

normally- plasma cells produce a wide range of igs, but in myeloma, malignant plasma cells produce an excess of one type of ig- paraprotein- usually igG and A

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5
Q

symptoms of myeloma

A

C- calcium raised (hypercalcemia symptoms due to increased ostecvlast bone resoption - bones, stones, abdo moans, pyshciatric grans

R- renal failure- hypercalcemia can cause renal stones, mainly - immunoglobulin light chain kappa can deposit in organs like kidneys- you get BENCE JONES PROTEIN IN PEE

A- anemia

B- bone leisions- increased osteoclastic activity causes boneache- backache is the most common syndrome

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6
Q

investigations for myeloma

A

fbc+ blood film- anemia, esr increase, + rouleaux formation

urine dipstick- BENCE JONES PROTEIN

u+e= renal failure

serum protein electropheresis: ig prarprotein M spike- hypergammaglobuliemia for that specific IG

xr of skull- pepper pot skull

osteolytic lesions of punchedout holes

BM biopsy- >10% plasma cells!

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7
Q

differential for hematology

A

MGUS- mammyloid gammopathy of undetermined significance- this is a precursor to myeloma but not myeloma itself. this is asymptomatic, has little paraprotein spile and <10% BM plasma cells

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8
Q

treatment for myelomas

A

chemotherapy, bisphosphates (ends in dronate), dialysis

consider bm stem cell transplant

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9
Q

whats an indolent lymphoma and give 3 subtypes

A

slow growing and advanced at presentation
incurable, death around 10 years later
follicular lymphoma
mantle cell lymphoma
CLL

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10
Q

what are the 2 types of lymphomas

A

hodgkins (speficic disease) and non hodgkins (the rest)

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11
Q

where do you find reed sternberg cells

A

Hodgkin’s lymphoma

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12
Q

causes of lymphomas

A

primary immunodeficiencies
secondary immunodeficiency- hiv, recipients of transplants
infection- ebv, helicobacter pylori
autoimmune disorders

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13
Q

general symptoms of lymphomas

A
  • lymphadoenopathy
  • b symptoms- fevers, drenching night sweat, appeptie loss
  • SVC obstruction
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14
Q

what are b symptoms you find in lymphomas

A

fever
unintentional weight loss
night sweat

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15
Q

side effects of chemo treatment for lymphomas

A

alopecia, infertility, nausea

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16
Q

what classification system is used for lymphomas + outline it

A

Lugano classification
emphasises weather the affected nodes are above or below the diaphragm

  • stage1- one node/ group of nodes
  • 2- >1 groupd of nodes but same side of diaphragm
  • 3- lymph nodes both above and below diaphragm
  • 4- widespread involvement including non lymphatic organs like lungs or liver
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17
Q

epidemiology of Hodgkins lymphoma

A
  • young adults- peaks in teens and early twenties, again after 70
  • previous epstein bar virus
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18
Q

presentation of Hodgkins lymphoma

A
  • b symtoms- fever, weightloss, night sweats
  • painless rubbery lymphadenopathy - WORSE AFTER DRINKING ALCOHOL
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19
Q

what are the investigations for hodgking lymphoma

A

lymph node biopsy!!- look for reed sternberg cells (diagnostic)

  • a variant- nodular lymphocyte predominant Hodgkin’s produces POPCORN CELLS

blood test- high esr, high lactasse degydrogenase (ldh), low hb

use ct/mri for chest/ abdo/ pelvis for staging

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20
Q

in lymph node biopsy for Hodgkins lymphoma what is the diagnostic feature to look out for

A

reed sternberg cells

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21
Q

treatment for Hodgekins lymphoma

A

chemo + radiotherapy

ABVD chemo

  • adriamycin
  • bleomycin
  • vindlastine
  • dacarbazine

(se= infertility)

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22
Q

presention of Non Hodgkins lymphoma

A

b symptoms- fever, weeight loss, drenching night sweats

painless rubbery lypadenopathy- NOT affected by alcohol

more varied and will affect more parts of the body

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23
Q

investigation for Non hodgkins lymphoma

A

lymph node biopsy- diagnostic- NO reed sternberg cells or popcorn cell

CT/ MRI chest, abdo, pelvis for staging

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24
Q

treatment for Non hodgkins lymphoma

A

depends on subtype- indolent/ low grade= watch and wait, alkylyting agents, combo chemo, radio

aggresive/ high grade:

chemotherapy

R-CHOP

  • Rituximab
  • Cyclophosphamide
  • Hydroxy-daunorubicin
  • O – Vincristine (oncovin is brand name)
  • Prednisolone
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25
Q

malignant clonal expansion of lymphocytes which occur at different stages of lymphocyte development- whats this

A

non hodgkins lymphoma

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26
Q

absence of reed sternberg cells- what does this show

A

non hodgkins lymphoma

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27
Q

what is myeolodysplastic syndrome and what can it transform into

A

form of cancer from mutation of myeloid cells in bone marrow- they now do inaffective haematopoesis- turn into myeloid leukaemia

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28
Q

what blood conditions does myelodysplastic syndrome cause

A

causes low level of blood components that originate from myeloid cell line
- anaemia - low hb
- neutropenia- low neutrophil count
- thrombocytopenia- low platelets

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29
Q

types of leukemia

A

-acute myeloid leukemia- rapid progression cancer of myeloid cell line
- chromic myeloid leukaemia- slow progresion
- acute lymphoblastic leukaemia- rapid progression of cancer of lymphoid cell line
- chronic lymphoblast leukemia- slow progression of above

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30
Q

down syndrome is associated most with what type of leukemia, also in children less than 6

A

acute LYMPHOID leukmia

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31
Q

what’s the difference between cells in acute and chronic leukaemia

A

acute- cells don’t differentiate at all
chronic- cells partially differentiate

32
Q

what is cytopenia

A

low levels of rbc or wbc or platelets (anaemia, leukopenia, thrombocytopenia)

33
Q

definition of acute myeloid leukemia

A

proliferation of myeloblasts- -so no basophil, neutrophil and eosinophil

34
Q

risk factors for acute myeloid leukemia

A

radiation, chemo

35
Q

presentation of acute myeloid leukemia

A

bone marrow failure-

  • neutropenia- less neutrophils
  • anaemia, - low hb
  • thrombocytopenia - less platelet

SWOLLEN GUMS

splenomegaly

36
Q

investigation for acute myeloid leukemia

A

fbc+ blood film- pancytopenia- deficiency of rbc, wbc, platelets

  • neutropenia
  • thrombocutopenia
  • anemia

cytology- AURER RODS (cytoplasmic aggregagte)

GS= bone marrow biopsy- >20% myeloid blasts

37
Q

treatment for acute myeloid leukemia

A

supportive treatment correcting anaemia, thromboctyopenia

chemo + allopurinol- prevent tumor lysis syndrome

38
Q

definition of chronic myeloid leukemia

A

overproduction of myeloid progenitor- which comes before the myeloblast

39
Q

pathophysiology of chronic myeloid leukemia

A

mutation in philidelphia chromosone- activation of tyrosine kinase- granulocytes divide too quickly- too many premature cells- accumulate in bone marrow

40
Q

presentation of chronic myeloid leukemia

A

MASSIVE SPLENOMEGALY

hyperviscosity- headaches, thrombotic events,

bone marrow faulure- neutropenia, anaemia, thrombocytopenia

b symptoms- wieght loss, night sweats, loss of apetite

41
Q

investigation of chronic myeloid leukemia

A

genetic testing for BCR ABL - philidelphia chromosome

bone marrow biopsy from iliac crest- shows increase in myeloid progenitors

fbc

42
Q

treatment of chronic myeloid leukemia

A

IMATINIB- inhibits tyrosine kinase

43
Q

definition of acute lymphoblastic leukemia

A

rapid proliferation of lymphoblasts

44
Q

risk factors/ epidemiology of acute lymphoblastic leukemia

A

children under 6

downs syndrome

radiation

45
Q

presentation of acute lymphoblastic leukemia

A

bone marrow faulure-

  • anaemia: lethargy and pallor
  • neutropaenia: frequent or severe infections
  • thrombocytopenia: easy bruising, petechiae

b symptoms- more common than aml

hepatosplenomegaly

SWOLLEN TESTICLES

46
Q

investigation inc diagnostic of acute lymphoblastic leukemia

A

bone marrow biopsy- >20% lymphoblasts (diagnostic)

blood film- increased lymphoblasts

47
Q

treatment of acute lymphoblastic leukemia

A

chemo

48
Q

what is chronic lymphoblastic leukemia

A

failure of cell apoptosis,

most common leukemia overall

49
Q

presentation of chronic lymphoblastic leukemia

A

asymptomatic

lymphadenopathy and bone marrow failure

50
Q

investigation inc diagnostic of chronic lymphoblastic leukemia

A

diagnostic= blood film- smudge cells!

51
Q

treatment for chronic lymphoblastic leukemia

A

chemo, pallitative if old

52
Q

complication of chronic lymphoblastic leukemia

A

richters transformation- b cells massively accumulate in lymph nodes- massive lympadenopathy and transformation from cll— agressive lymphoma

53
Q

size of microcytic anemia

A

<80fcv

54
Q

what is the size of anemia based on

A

mean copuscular volume- average size of rbc

55
Q

types of microcytic anemia

A

thalassaemia (hemolytic)
anemia of chronic disease
iron deficiency
lead poisoning
sideroblastic

56
Q

where is iron absorbed

A

duodenum and upper jejunum

57
Q

what is iron bound to to travel

A

transferrin

58
Q

what is iron stored as

A

ferritin

59
Q

features of anemia

A
  • Peripheral coldness
    • conjuctival pallor
    • tachycardia
    • fatigue``
    • brittle hair
    • exertional dyspnoea
60
Q

what protein facilitates fe absorbtion

A

transferrin

61
Q

causes of iron deficiency anemia

A

diet/ malnutrition= not enough red meat/ beans- vegan?
malabsorptibe conditions- coeliac, ibd
bleeding- colorectal cancer, menstruation
pregnancy- a lot os transferred to foetus
kids- increased requirement

62
Q

pathophysiology of iron deficiency anemia

A
  • fe is usually absorbed and circulates bound to transferrin, stored as ferritin or incorporated into heamoglobin
  • in iron deficiency- less iron available for haem synthesis- so less haemoglobin- so lack of effective rbc- so anemia
63
Q

spefici signs and symptoms of iron deficiency anemia

A

symptoms:
- tired
- cold
- palpitations

signs:
- koilonychia - spoon shaped nails
- angular stomatitis- ulceration at mouth corners
- atrophic glossitis- tongue enlarged

64
Q

investigations for iron deficiency anemia

A

fbc and blood film- microcytic anemia
fe studies- low serum fe, low ferritin, low transferrin saturation, high TIBC
blood film- rbc different size and shapes
reduced reticulocyte count

65
Q

treatment of iron deficiency anemia and se of it

A

oral ferrous sulphate- side effect of black stool and diarrhea
if poorly treated then consider ferrous gluconate

66
Q

thalassemia- is it genetic?

A

yes- autosomal recessive , genetic defect in the protein chain that makes up hb

67
Q

where is thalassaemia prevelant

A

where malaria is- south asia, india, middle east

68
Q

alpha and beta thallasemia have what chromsomes and genes altered

A

alpha- deficiency in alpha globin gene, deletion on chromosme 16
beta- deficiency of beta globin gene, mutation on chromosome 11

69
Q

presentation of thalassaemia

A

chimponk face- massively enlarged forhead and cheekbones
hepatospleenomegaly
ruq pain
gallstones
failure to thrive
may get jaundiced

70
Q

investigations for thalassaemia

A

HB electropheresis!! (diagnositc)- see high HbA2 (beta) and Hb H (alpha)

FBC- microcytic anemia
Blood film- recitulocyte count (increased) and hypochromic rbc

71
Q

treatment for thalassaemia

A

regular blood transfusion + iron chelton therapy
splenectomy
+ folate supplements
+ bm stem cell transplant

72
Q

sideroblastic anemia- what is it and who is affected most, what is it caused by, what is it

A

x linked inherited congenital condition, mainly affecting boys
caused by excess alcohol intake, vitamin B6 deficiency, lead poisoning
lack of mature rbc, and too much iron so irons not used in hb synthesis and stays trapped in mitochondira
build up of iron and low haem

73
Q

investigation for sideroblastic anemia

A

FBC AND BLOOD FILM- microcytic with ringed sideroblasts (iron deposits)
FE STUDIES- increased fe, increased ferritin, raised transferrin sats, low TIBC

74
Q

what IS thalassemia

A

decreased rate of production or no production of one or more globin in chain in the red cell precurosirs or mature red cells

75
Q
A

2a systems (7 decks)

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