Haematology in systemic disease

Question 1

changes to the b in systemic diease

Answer 1

• 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)

Question 2

A of chronic disease

Answer 2

• inflammatory mediators (FE2+)
• epo dysfunctional
• reduced life span of RBC

Question 3

A of CD eg.

Answer 3

• bronchitis
• RA
• IBD
• TB

Question 4

main source of iron?

Answer 4

recycling iron from macrophages , involves ferroportin

Question 5

what is hepcidin regulated by?

Answer 5

• HFE gene
• transferrin receptor
• inflammatory mediators

Question 6

RA

Answer 6

• increased inflammatory mediators wc c ^ hepcidin wc inhibits ferroportin so less fe2+ leaves funtinonal iron deficiency

Question 7

A of chronic kidney disease?

Answer 7

• 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

Question 8

fistula

Answer 8

connection between artery and veins

Question 9

uraemia

Answer 9

• high urea contents (b usually removed by kidney) inhibits megakaryocytic leading to decreased platelet
• look at their platelet, ck, abc count

Question 10

how to treat CKD

Answer 10

• underlying disease
• give recombinant human EPO
• make sure vit b12 and folate levels are normal
• transfusion if really bad

Question 11

NICE guideline to look for iron defeiceny

Answer 11

• use reticulocyte count
• if count <200microg
• give IV iron

Question 12

possible haematological abnormalities in kidney disease

Answer 12

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

Question 13

RA

Answer 13

• AB of skin
• swan neck deformitiation
  lateral deviation of the fingers
  boutoin

Question 14

treatment of RA

Answer 14

• 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

Question 15

felty’ssyndrome

Answer 15

• large spleen
• low netrophpenia d splenomegaly destruction of WBC, + failure of the bone marrow to. make them b they become insentive to GCSF

Question 16

Liver disease

Answer 16

-hypotension in portal system wc c splenomegalia d back pressure so overactive removal of the cells c low b count

Question 17

features of

Answer 17

• 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

Question 18

what do they become deficient of early on

Answer 18

vit k

Question 19

thromboyctponia ever diseas

Answer 19

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

Question 20

alcohol

Answer 20

• 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….

Question 21

post operative reactive changes

Answer 21

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

Question 22

infection

Answer 22

• RBC = chronic can.c haemolytic anaemia (malaria)
• ^WBC neutropenia (lympsytosis = viral / eosinophila)
  neutropenia (sepsis)
  -thrmocyt;

Question 23

DIC

Answer 23

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 )

Question 24

cancers (not affecting the bone marrow

Answer 24

• 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

Question 25

risk of cancer p

Answer 25

• venous thrombosis (wc ^ risk embolism stroke)

Question 26

leucoerythoblastic film

Answer 26

• 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