Haematology Flashcards
how does growth hormone deficiency lead to obesity
The reduction in GH secretion may further increase fat accumulation by reducing lipolysis, and therefore exacerbate obesit
32yr old man - TB therapy - microcytic anaemia with low HB , raised ferritin transferrin sat and serum iron - basophilic granules seen on film what dx
sideroblastic anaemia
when in anaemia do you get signs of hyper dynamic circulation such as raised HR , flow murmurs and HF
when HB unver 8
well known drug cause of sideroblastic anaemia
isoniazid
causes of iron defiency anaemia
malabsoprtion - eg coeliac
BLood loss - menorrhagia , GI
hookworm
malabsorption bloods what is shown - electrolytes
ix and Mx for iron def an.
Ix
FBC, blood film, iron studies, Gi ix, menorrhagia
treat cause and replace iron stores for 3 months with PO fe - aware of se such as gi disturbance and black stools
27yr old vegan woman - weakness of legs and numbness and paraesthesia. reflexes present and plantars upgoing . romberg positive - dx?
subacute degeneration of the cord
ALS - no sensory
MS - not gradual - flares and remissions
vit E - not as common
what are megaloblasts
large immature RBCs and also hypersegemented neutrophils over 5 on blood film
caused by inhibtion of DNA synthesisi - folate and B12 needed for this
4 meagloblastic an cuases
B12 , folate, methotrexate and hydroxyurea
no megaloblasti cmacrocytsis cx
alcohol
hypothyrodisim
myelodysplastic syndromes
reticulocytosis
60 man - hernia repars, HB 19.2, platlet 490, mild splenomegalym and red complexion - raised cell mass and EPO level normla. what dx
VTE
this is polycythaemia rubera vera
not high Ca - associated with myeloma not PCV
hypouricaemia - tumour lysis syndrome
cor pulmonale
mutuation with polycthaemia
jak2
difference between primary and secondary polycythaemia
primary - normal or low EPO
secondary - high EPO
primary polycthaemia what cause
neoplastic - polcythaemia vera
secondary polycthaemia could be what
repsonse to hypoxia, neoplasma or cysts
chronic cause
ix for polycythameia
hb and plasma cell vol - both up
mx of PCV
venesection
hydroxyurea - suppress production
aspirin - reduce platelet aggregation and occlusion.
36 F, SOB and pleuritic CP, PE dx, PMH of antiphospholipid syndrome adn DVT 10m ago - on warfarin. What is appropriate long term mx plan
warfarin for life, target INR of 3-4 ( normal VTE target 2-3- so in this case tx failure)
provoked PE
3m tx
unprovoked pe
6mon
recurrence target INR
3-4
28
fatigue and SOB
recent penumonia - mycoplasma
red-brown urine
icteric - jaundiced
Hb 98
normal WCC and platelete
pre-hepatic hyperbilirubinaemia and raised LDH
what is this?
autoimmune intravascualr haemolysis
raised LDH
haemolytic anaemia - rbc contain LDH
mycoplasma is a common cuase of what
cold autoimmune haemolysis
different types of haemolytic anaemia
hereditary and acquired
H - h. spherocytosis
metabolism - G^PD and pyruvate def
Hb - sickle cell, thalsassaemic, HBc
acquired
immune - autoimmune - warm/cold
alloimmune
red cell frag
infections such as malaria and clostridia
secondary to renal or liver disease
nocturnal
autoimmune causes differnces between warm and cold
warm - antibodies bind at body temp - centrally haemolytic - iGg - lymphoma, drugs and SLE
cold- normal in peripherals and binding occurs here under 4 degrees - Igm - infections usch as mycoplasma and EBV
steriods treat
75m
asx but mildly anemic
PMH - HTN, AF, metallic arotic valve
Hb 106 normocystic , uncoguated hyperbilirubinaemia
high LDH
reitucloytes on film
most likely cause?
haemolytic anaemia
how do you distinguish between an immune and non immune haemolytic anemia
coombes test
positive in immune
30F , fatigue, WL and menorrhagia. Easy bruising, HB 8 WCC of 30 and platelets of 40. Prolonged PT and APTT and low fibrinogen, raised d-dimer - which blood film consistent with most likely dx
auer rods - APL
clotting disorder looks like DIC
AML with DIC is APL - get auer rods on film
smudge cell
CLL
mx of AML
anaemia
thrombocytopenia
DIC
infection
TLS - cell breakdoen
CNS prophylaxis
packed RBC
platelts if udner 10
FFP cryo
ABx and reverse barriernurising
allopurinol
intrachecal chemo such as methotrexaae
vWD what pattern on clotting tests
normal platelets and normal PT and TT
prolonged bleeding and prolonged APTT
vWF factor nromally linkes platelets to exposed endothelium and stabalises clotting factor
8 - which is why APTT prologned in due to decreased factor 8 activity
in contrast to haemophilia, bleeding into joints or muscles is uncommon
64yr old man - high ant resection for ca - post op hb of 68. SON - tranfuse - 2 units - develops fever at 37.7 - obvs normall what do you do
slow down transfusion and consider paracetamol - as for febrile non-h transfusion reaction
TACO presents with fluid overloads hwo to manage
slow transfusion and give furosemide
acute haemolytic transfusion reaction caused by giving incompatible blood how to manange
can develop to dic
stop transfusion and give saline and manage DIC
5yr old male - fever headache and skin rash. ,ICU - blood oozin from cannula sites, gingival bleeding and low bP - what coag profile most liekly seen
decreased fibrinogen, decreased platelets, elevated d-dimer
sounds like DIC secondary to meningitis
- DIC lots of clotting happenin and using up all platelts and fibrinogen and because clotting d-dimer will rise as breaking it all down, Therefore normal function does not occur so bleed
how does DIC present
inappropriate activation of clotting cascade resulting in thrombus formation and depletion of clotting factors and platelets. Pt presents with excess bleeding
petechiae, bruising and confusion and low BP
RF - major trauma, burns, sepsis, obstetric complications, solid tumour or haematological malignancies
1m hx back pain and fatigue in 75M. IgG paraprotein spike and urinary bene jones protein spike what complication of dx
hypercalcaemia
myeloma features
evidecne of organ damage– CRAB HAI - hyperCa, renal impair, anaemia, bone disease, hyperviscoity, amylodiosis, infection(recurrent)
ix for myeloma
FBC, film, ESR, urine dip, 24hr urine collection, UandEs , urate, albumin, calcium, phosphate, ALP, serum and urinary electrophoresis. serum ig , X-ray and bone marrow biopsy
amyloidosis what is it - can get in myeloma too
where do you take biopsy from
deposition of extraceullar insoluble fibrins in organ and BV
macroglossia( large toungue), hepatosplenomegay, neuropathuoes
take biopsy from the rectum( chritz jeuger - tonsils)
80M , 3rd admission in 6m with LRTI requiring IV. course exp creps at base with consolidation on CXR - WCC 47 - dx?
CLL - can watch and wait, severe can chemo
what is richters syndrome
CLL turn into high grade lymphoma
usually asx in CLL
causes of massive splenomegaly - MS
CML
myelofibrosis
malaria
visceralleishManiasis
what drug causes low magnesium and low calcium and sodium
omeprazole
malnutrition causes what electrolytes to be low
Phosphate and magnesium
what flow murmur
Blood flowing faster than normal through the heart valves
When it occurs
During exercise, pregnancy, rapid growth, or other times when blood flow increases
Who it affects
Common in children and teens, but some people experience them into adulthood
what are the two types of lymphoma
Lymphoma is the malignant proliferation of lymphocytes which accumulate in lymph nodes or other organs. Lymphoma may be classified as either Hodgkin’s lymphoma (a specific type of lymphoma characterized by the presence of Reed-Sternberg cells) or non-Hodgkin’s lymphoma (every other type of lymphoma that is not Hodgkin’s lymphoma).
what is more common hodgkins or non hodgkins
Non-Hodgkin’s lymphoma is much more common than Hodgkin’s lymphoma
NonH sx
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)
Lymphadenopathy in Hodgkin’s lymphoma can experience alcohol-induced pain in the node
True
B’ symptoms typically occur earlier in Hodgkin’s lymphoma and later in non-Hodgkin’s lymphoma
True
Extra-nodal disease is much more common in non-Hodgkin’s lymphoma than in Hodgkin’s lymphoma
true
non h tx
Rituximab is used in combination with conventional chemotherapy regime
screened for hep B as rituximab can cause reactivation
hodgkins features and signs
lymphadenopathy - alcohol
systemic b sx
mediastinal mass
nromocytic anaemia
esoinophilia
LDH raised
lymph node biopsy showing multinucleated or bilobed nucelus with eosoinophlic inclusion