Heme Flashcards
effect of PTT in lupus anticoag
prolonged
first dx step towards SVC syndrome?
CXR
-most commonly caused by malignancy
trousseaus sign
migratory thrombophblebitis most highly assoc with pancreatic cancer but can be others as well
CML vs leukomoid reaction
CML has a low LAP and more myelocytes
- CML has absolutely basophilia
- CML has extreme leukocytosis*****
- philadelphia csome
polycycthemia vera and leukomoid reaction both show elevated LAP score
features of CLL
- 70
- fatigue, splenomegaly
- mature lymphocytsis and smudge cells on smear
- if found incidentally and asx, don’t treat –> very slow growing
- thrombocytopenia –> late finding, poor px because shows impaired BM fx
tumor lysis syndrome labs, tx
- INC K, Phos
- dec Ca
- AKI
first line is IV fluids, then allopurinol
physical exam signs of hemolysis
splenomegally
jaundice
scleral icterus
AML
age ~60
- can have variable white count
- inc myeloblasts with pancytopenia
- myeloperoxidase +
- auer rods
- 15;17
- all trans retinoic acid
Young guy with no clot risk develops DVT. You give high dose heparin for DVT in patient with prolonged aPTT but nothing changes, including aPTT. What’s happening?
ATIII deficiency
- AD
- heparin requires ATIII to work –> then deactivates II, X
first diagnostic steps in malaria?
thick smear –> followed by thin smear
exercise hemoglobinuria is what type of hemolysis?
intravascular
***of note, haptoglobin is usu normal in extravascular hemolysis
Kehr’s sign
referred left shoulder pain from splenic rupture
philadelphia csome
9;22
tx with imatinib (tyrosine kinase inhibitor)
> 90% in CML but can be in ALL with kiddos so watch out
acute trauma coagulopathy
admin pRBC, FFP and plt in 1:1:1
dactylitis
swelling of hand or feet assoc with vasoocclussive crisis
also seen in RA, sarcoid
p falciparum proph
atovoquone-proguanil
Falcip is resistant to chloraquine in endemic areas
***ring inclusions in RBC
Coombs results
positive= HS!
Negative= AIHA
**they both have spherocytes on smear
bilateral patchy infiltrates on CXR, dry cough, hemolysis labs? dx? test?
cold, IgM, AIHA
positive direct coombs
isolated fever within hour or two of recieving blood products
normal labs = non hemolytic transfusion rxn, can give acetaminophen
next step–> check coombs
parvovirus B19
pancytopenia
hypocellular, fatty marrow on biopsy
thrombocytopenia in cirhossis most likely caused by?
hypersplenism
spleen gets large due to inc portal pressures –> sequestrs platelets
tx for refractory ITP that does not respond to IVIG/ steroids
splenectomy
PTT is what pathway
intrinsic
*affected by heparin
what is THE BEST TEST EVER for hereditary spherocytosis
- also, what should you give them as proph?
- what pathology are that at risk for at a younger age then usual?
ema (eosin-5-m…) binding test, it uses flow
characteristics of HS: inc RDW, inc MCHC, hemolysis signs
- proph with folic acid to prevent megaloblastic anemia
- gallstones
safe malaria proph in pregnancy
mefloquin
atovaquone- proguanil
paroxysmal nocturnal hemoglobinuria
genect defect in anchoring protein
at risk form thrombosis in atyplica locations
test= CD55/CD59
polycythemia vera
hyperviscosity sx
- can cause essetnail thrombocytosis
- can cause 2nd gout
tx= phlebotomy
characteristics of hodgkins (don’t forget the paraneoplastic syndrome)
- reed sternberg cells= polynuclear giant cell, CD15/30+
- EBV
- alcohol induced pain in lymph nodes
- painless cervical lymphadenopathy
- elevated ESR is assoc with poor px
- paraneoplastic syn: inc Ca++ via ectopic 1a-OH production
tx with chemo
malarial endemic regions
asia, africa, south america
signs can look like hemolysis so look at history
diamond blackfin anemia
- dx at <1 year –> definitive is bone marrow bx
- macrocytic anemia (lack other cytopenias)
- triphalangeal thumbs
tx of CLL
if asyx –> observe and monitor progression
if sx –> rituximab (anti CD20)
PE signs assoc with Fe deficiency
koilonychia- SCOOPED NAILs
angular chelitis
tx of ALL
(ab= CD10, CD19, tdt)
- aggressive chemo with vincristine, imatinib if 9;22
- CNS proph with intrathecal chemo
differentiate megaloblastic from simply macrocytic
megaloblastic = hypersegmented neutrophils
-can only be caused by b12/ folate defi
antibiotics in sickle cell crisis/ sepsis?
IV ceft –> improved mortality
think of coverage for staph, salmonelloa, e coli, s pneumo (functional asplemia)
presentatin seems consistent with G6pd and HS. How do you differentiate?
G6PD is more acute, 2-3 days after oxidative stress insult, like abx
HS happens a few weeks later and has ** inc MCHC**
hair cell luekemia
common in older men with similar presentation to CLL
- massive splenomegaly
- TRAP+ (tart tresistant acid phos), CD11c
- dry BM tap
- tx= cladribine
vWD labs and tx
inc PTT (dec factor VIII) **hemophilia will also have long ptt
inc bleeding time
nl plt
tx with desmopressin
(VIII is part of extrinsic pathway, requires vwb)
more rare side effect of TMP-SMX that you don’t think of as often?
agranulocytosis
lab disturbances that can be seq of gestational dm in newborns?
hypoglycemia
hypocalcemia
polycythemia
ringed sideroblasts, microcytic vs macrocytic anemia
microcytic= lead poisoning
macrocytic= myelodysplastic syn
warf vs DOAC in acute DVT?
DOAC acts instantly
warf induced skin necrosis
due to relative Prot C deficiency which is the first factor to decrease
heme effect of isoniazid
acq sideroblastic anemia that ,masquerades as fe def.
- inhibits pyridoxine req for protoporphyrin synth
- dimorphic rbcs
- INC fe, DEC tibc
lab values in vaso-occlusive crisis
aka splenic sequestration
- reticulocytosis
- thrombocytopenia
- normocytic anemia
