Heme/Onc (F.A) Flashcards
erythrocyte lifespan
120 days
platelet lifespan
10 days
what is the vWF receptor on platelet?
Gp1b
what is the fibrinogen receptor on platelet?
GIIb/ IIIa
what is the order of leukocyte/ WBC differential
Neutrophils (60%) Lymphocytes (30%) Monocytes (6%) Eosinophils (3%) Basophils (1%) "neutrophils like making everything better"
what does a neutrophil look like normally
multilobed
hypersegmented neutrophil indicates? (6+ lobes)
megaloblastic anemia (folate or B12 deficiency)
band cells?
immature neutrophils. increased number suggestive of increased myeloid proliferation (infection or CML)
what are factors that attract neutrophils
c5a, LTB4, kallikrein, PAF, IL8
monocyte appearance?
large kidney bean nucleus
frosted cytoplasm
precursor to macrophage
what activates a macophage
gamma-interferon
jobs of a macrophage
(1) phagocytose
(2) APC- via MHC II
explain pathophys of sepsis
Lipid A in bacterial LPS (or LOS in Nisseria) bind CD14 on macrophages initiating septic shock (which goes on to cause greater inflamm/ cap perm, etc.
what does an eosinophil look like
bilobate nucleus with large eosinophilic granules
what causes eosiniphilia
neoplasm asthma allergic process chronic adrenal insuff. parasite (helminth)
NAACP
what causes basophilia (very uncommon)
CML- myeloproliferative disease
what do basophils release?
heparin (for anticoag) and histamine (vasodilation)
also leukotrienes
how do mast cells degranulate
they bind IgE via Fc portion, and attach it to the membrane..upon coming across an antigen, the IgE will crosslink –> degranulation
what type of HS reaction is mast cells involved in?
HS Type 1
dendritic cell functions
(1) highly phagocytic
(2) APC- via MHC II amd Fc receptors (B7) .. link between innate and adaptive immunity (bc constantly sampling and presenting)
what cells are lymphocytes
B, T, NK
have lg nucleus size of RBC
Bcell markers
CD19, CD 20, CD 21
what can B cells do
(1) become plasma cells and produce ab
(2) live as memory cells
(3) act as APC - via MHC II
80% of circulating lymphocytes are
T cells
T cell functions
(1) cytotoxic T cells– CD8+ that respond to MHC I
(2) helper T cells– CD 4+ that respond to MHC II
[ remember “rule of 8”, and both express CD3]
(3) regulatory T cells
what is necessary for T cell activation?
CD28
what does a plasma cell look like
clock face chromatin
well developed golgi apparatus , abundant RER
eccentric nucleus
(found in marrow not usually blood)
name the locations of fetal/ adult erythropoeisis
(1) yolk sac – 3-8 wk
(2) liver – 6 wk till birth
(3) spleen – 10-28 wk
(4) bone marrow– 18 wk till forever
“ Young Liver Synthesizes Blood”
adult hemoglobin
HbA1 – 2alpha, 2beta
HbA2 – 2 alpha, 2 delta (rare, only seen increased in B-thal)
fetal hemoglobin
HbF– 2 alpha, 2 gamma
remember “ always alpha, gamma goes, becomes beta”
HbF vs HbA
HbF has greater oxygen binding avidity, therefore it is able to steal O2 from mother’s HbA.. this is because HbF has weaker binding to 2,3 BPG
universal PLASMA donor
AB type
universal BLOOD donor
O type
universal PLASMA acceptor
O type
universal BLOOD acceptor
AB type
anti- A and anti- B are what type of antibodies
IgM (can’t cross placenta)
IgM stays in Mom
anti-Rho (aka anti D) is what type of antibody
IgG (CAN cross placenta)
IgG can Go to baby
Rh hemolytic disease of the newborn: mom status? baby status? path? t(x)?
mom= Rh neg
baby 1= Rh pos
baby 2= Rh pos, gets hemolytic disease
– upon delivery of 1st Rh+ baby, mom makes anti-IgG against D antigen. when carrying 2nd baby, IgG crosses placenta causes hemolytic d(x)
t(x)- RhoGAM- an exogenous anti-D IgG to prevent MATERNAL production of anti-D IgG
Hemoglobin electrophoresis migration: from farthest to shortest distance migrated
HbA, HbF, HbS, HbC
“a fat santa claus”
why? bc HbS (has val not glutamic acid) so it is neutral
HbC (has lysine not glutamic acid) so it is positive
HbS
in B chain, a valine is there instead of glutamic acid. makes a neutral pocket that can allow RBC polymerization and sickling
HbC
in B chain, a lysine (+) is there instead of glutamic acid (-). not as severe as HbS bc no sickling
PT measures which coagulation pathway
Extrinsic
PTT measures which coagulation pathway
Intrinsic
What factors are in EXtrinsic pathway
VII
What factors are in INtrinsic pathway
XII, XI, IX, VIII
what is Factor II known as
Prothrombin, active= Thrombin
What is Factor I known as
Fibrinogen, active= Fibrin
what activates prothrombin to thrombin
Factor Va
what activates fibrinogen to fibrin
factor IIa, thrombin
intrinsic pathway is activated by
subendothelial collagen
extrinsic pathway is activated by
Tissue Factor
what degrades fibrin
plasmin
Hemophilia A- def?
Hemophilia B- def?
Hemophilia C- def?
mode of inheritance?
A- VIII —- XR
B- IX —– XR
C- XI —– AR
role of vit K epoxide reductase
reduces vit K. reduced vit K is a cofactor to gamma glutamyl carboxylase which activates factors: II, VII, IX, X, prot C, prot S
role or protein C and protein S
anti-coag!
inactivate Va, and VIIIa
explain the steps of primary hemostasis
(1) endothelial damage– vasoconstriction
(2) VWF (from WPB and platelets) bind exposed collagen
(3) “adhesion”- platelets bind VWF via Gp1b which causes platelet release of ADP and TXA2
(4) “activation” - ADP induces GIIbIIIa on platelets
(5) aggregation- fibrinogen binds platelets at GIIbIIIa and links platelets
what does Ristocetin do?
activates VWF to bind Gp1b on platelet
acanthocyte= spur rbc
- liver disease, abetalipoproteinemia
basophilic stippling
lead poisoning, siderblastic anemia, myelodysplastic syndrome
found in blood stream
teardrop cell
bone marrow infiltration (myelofibrosis)
bite cell
G6PD
Burr
ESRD, liver disease, pyruvate kinase def
ringed sideroblast
sideroblastic anemia, excess iron in mitochondria, seen in bone marrow
schistiocyte= helmet cell
TTP, HUS, DIC, HELPP, mechanical valve
target cell
"HALT" HbC Asplenia Liver Disease Thalassemia
Heinz bodies
G6PD (sign of oxidation of sulfhydryl group deposited, leads to bite cell formation)
Howell-Jolly Bodies
asplenia.
nuclear remnants not removed by spleen macrophages
