Haematology in systemic disease Flashcards
changes to the b in systemic diease
- multifactorial
- IL-6 / TNF a/IFN-y c ^hepacidin vFe2+ released (RA)
- (gastritis/UC) GI issues since you cant absorb and bleeding so ^ RBC macro
- drugs (NSAIDs/antacids)
A of chronic disease
- inflammatory mediators (FE2+)
- epo dysfunctional
- reduced life span of RBC
A of CD eg.
- bronchitis
- RA
- IBD
- TB
main source of iron?
recycling iron from macrophages , involves ferroportin
what is hepcidin regulated by?
- HFE gene
- transferrin receptor
- inflammatory mediators
RA
- increased inflammatory mediators wc c ^ hepcidin wc inhibits ferroportin so less fe2+ leaves funtinonal iron deficiency
A of chronic kidney disease?
- reduced EPO d kidney damage and so reduced clearance of hepcidin and ^ hepcidin produced by inflammatory mediators + EPO v so less fe2+ is being used to make RBC
- reduced lifespan of RBC as direct effect of uramemia
fistula
connection between artery and veins
uraemia
- high urea contents (b usually removed by kidney) inhibits megakaryocytic leading to decreased platelet
- look at their platelet, ck, abc count
how to treat CKD
- underlying disease
- give recombinant human EPO
- make sure vit b12 and folate levels are normal
- transfusion if really bad
NICE guideline to look for iron defeiceny
- use reticulocyte count
- if count <200microg
- give IV iron
possible haematological abnormalities in kidney disease
RED = anaemia / CKD/ blood lord/ can her/dietary causes
s
- neutrophils ; neutropenia (d immunosuppression or autoimmune KD) neutrophilic ( inlfammaltio / infection/ steroids c ^)
-platelets ; thrbocytopenia (d uraemia inhibits megakoryoctes
RA
- AB of skin
- swan neck deformitiation
lateral deviation of the fingers
boutoin
treatment of RA
- anti-inflammatory drugs
- paracetamol
- DMARDS ; wc slows down the development of the hand features
- firs steroids then chemo drugs
- also monoclonal antibodies against cytokines
SIDE EFFECT; gastritis d the the steroids , also autoimmune hypolytic anaemia
- throcytothemia d infection and hypersplenism
felty’ssyndrome
- large spleen
- low netrophpenia d splenomegaly destruction of WBC, + failure of the bone marrow to. make them b they become insentive to GCSF
Liver disease
-hypotension in portal system wc c splenomegalia d back pressure so overactive removal of the cells c low b count
features of
- back pressure goes all the way other gut causing GASTRIC VARICES (dilated veins prone to bleeding d to higher than normal pressure)(common in alcoholic liver disease)
- b loss contributed to by deficiencies of coagulation factors(since they’re made in the liver) / endothelial dysfunctional (d production of fat that contribute to membranes) / thrombocytopenia (b GSCF made in the liver) / defective platelet function
what do they become deficient of early on
vit k
thromboyctponia ever diseas
75% have it
- TARGET CELLS : (red outside, white then red dot) ^ cholesterol to phospholipid ratio so get target cells
- v platelet count d v THRMOBPOEITN made in liver
alcohol
- excess= directly toxic to bone marrow cells contribute to pantocytopnia
-secondary malnutrition (vit 12 and folate)
-viral hepatitis = b bone marrow failure can develop after an episode of hepatitis (hypoplatic/aplastic marrow)
-autoimmune
(thrmocoytes glycolic GP….
post operative reactive changes
Anaemia - d bloss pre and post - temporary polycythemia ; dehydrated WBC -neutropenia ; septic state - neutrophilic ; post op reaction/ b loss/ infection PLATELE - cytoina. ; drugs/steroids ?DIC - cytosis ; post op reaction/sepsis/DIC/bleeding
infection
- RBC = chronic can.c haemolytic anaemia (malaria)
- ^WBC neutropenia (lympsytosis = viral / eosinophila)
neutropenia (sepsis)
-thrmocyt;
DIC
disseminated intravascular coagulation
- pathological activation of coagulation (therefore ^ b .clots again and again and again)
- multiple little b clots forming = micro thrombi (uses up fibrinogen, co factors)
schistocytes d fragmented B cells b they get hurt as they get past these b clots
- so end up with long clothing time/ low fibrinogen/ evidence of activation of clotting system
- low platelet (d ^clotting used up elsewhere )
- can end up who acute kidney D and stroke (d renal stenosis )
cancers (not affecting the bone marrow
- RBC ; anaemia d bleeding/treatment(like chemo affects the bone marrow so cant make these cells)/ malnutrionment v iron)
- polycthemia ;cancers kidney c EPO producing tutors
- WBC ; neutropenia; (v vulnerable to sepsis )- bon emarrow infiltrated by cancer cells - chemo
- neutrophilia ; inflammation/infection
- platelets ; tcytopenia = chemo -sepsis, Dic, marrow infiltrated
- thrombocytosis ; inflammation, infection, bleeding, iron defieicny
risk of cancer p
- venous thrombosis (wc ^ risk embolism stroke)
leucoerythoblastic film
- b film showing immature red and white blood cells
- happens in sepsis/ severe megaloblastic anaemia / primary myrelofibrosis (with tear drop RBC)/ leukaemia /storgae disorders / bone marrow infiltration
