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path 2 exam 2 Flashcards

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1
Q

every 5-6 keratinocytes there is…

A

1 melanocyte
if there is more, can indicate neoplasm or reactive condition

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2
Q
A
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3
Q

what is excoriation?

A

traumatic lesion breaking down the epi

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4
Q

what is lichenification?

A

thickened rough skin (psoriasis_

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5
Q

what is a macule, patch?

A

circumscribed FLAT lesions
up to 5 mm, distinguished by coloration

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6
Q

what is onycolysis?

A

separation of nail from nail bed (traumatic, fungal, infection, blood clot)

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7
Q

what is a papule, nodule?

A

elevated dome-shaped or flat-topped lesions

nodule - spherical contour
greater than 5 mm
if nodule is shiny, could indicate basal cell carcinoma which is common in older pxs in sun exposed areas

papule - 5 mm or less

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8
Q

what is a plaque?

A

elevated flat topped lesions
greater than 5 mm

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9
Q

what is a pustule?

A

pus filled raised lesion

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10
Q

what is a scale?

A

dry, plate-like excrescence

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11
Q

what is a vesicle/bulla/blister?

A

fluid filled raised lesion
greater than 5 mm

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12
Q

what is acanthosis?

A

diffuse epidermal hyperplasia (epi is going DOWNwards)

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13
Q

what is dyskeratosis?

A

abnorm premature keratinization below the SG

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14
Q

what is ballooning?

A

INTRAcell edema of keratinocytes

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15
Q

what is hypergranulosis?

A

hyperplasia of SG

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16
Q

what is hyperkeratosis?

A

thickening of the SC
often associated with qualitative abnormality of keratin

seen in benign and malign lesions (squamous cell carcinoma, viral warts in female genital tract, condylomas)

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17
Q

what is lentiginous?

A

linear prolif of melanocytes

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18
Q

what is papillomatosis?

A

surface elevation of epi (epi is going UPwards) caused by hyperplasia and enlargement of contiguous dermal papillae

ex: viral wart, HPV induced
ROUGH PEBBLY type lesions

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19
Q

what is parakeratosis?

A

keratinization with RETAINED nuclei in the SC

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20
Q

what is spongiosis?

A

INTERcell edema of keratinocytes

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21
Q

what is an ulceration?

A

discontinuity of skin showing compelte loss of epi

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22
Q

what is vacuolization?

A

formation of vacuoles within or adjacent cells

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23
Q

what is acantholysis?

A

loss of intercell connection resulting in loss of cohesion between keratinocytes

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24
Q

what is the pathogenesis of utricaria?

A

mast cell dependent, IgE dependent –> exposure to Ag causing type I hypersensitivity (Ag binds to IgE)

mast cell dependent, IgE independent –> ex: drug induced utricaria like opiates and antibiotics, directly cause mast cell degranulation

mast cell independent, IgE independent –> caused by direct exposure to chemicals or drugs like aspirin induced

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25
which acute eczematous dermatitis cannot be removed?
atopic dermatitis
26
what is the pathogenesis of psoriasis?
strong association btwn psoriasis and ****HLA-Cw*0602**** T cells may create a CYTOKINE SOUP that leads to local inflam response that is responsible for psoriatic lesions
27
what are the squamous cell adhesion molecules?
dsg 1 in all epi layers dsg 3 in the deep epi layers BPAG 1 and 2 on the BM anchoning the epi into the BM and dermis
28
what is the pathogenesis of a nevi?
many have acquired mutations in BRAF or NRAS oncogene induced senescence is why many nevi do not progress into malig melanoma activation of RAS and BRAF causes prolif in a limited period followed by permanent growth arrest mediated by accumulation of p16/INK4a**** (melanomas lack this phase)
29
what is the pathogenesis of melanoma?
most important predisposing factor is SUN EXPOSURE leading to DNA damage most freq muts are ones affecting cell cycle control, pro-growth paths and telomerase muts that disrupt cell cycle control genes - CDKN2A gene is mutated in abt 40% of familial melanomas (AD)
30
what is the pathogenesis of malig melanoma?
sporadic melanomas show aberrant increase in RAS and PI3K/AKT signaling muts in BRAF are seen in 40-50% of melanomas also muts in NRAS muts that activate telomerase
31
what is the pathogenesis of SK and acanthosis nigricans?
activating muts in FGFR3 in many sporadic seborrheic keratoses muts in FGFR3 in familial form of acanthosis nigricans
32
what is the hematopoietic system composed of?
blood bone marrow thymus spleenn lymph nodes other hematolymphoid tissues
33
what are the different hematopoiesis cells types and their lifespan?
RBC = 120 days, 175 billion neutrophilic granulocytes = 7 hours, 70 billion platelets = 8.5 days, 200 billion
34
what are the sites of extramedullary hematopoiesis?
liver, spleen, lymph nodes, and soft tissue
35
explain reticulocytes
no nucleus stain with methylene blue which highlights residual RNA increased in conditions with increased RBC production and vice versa SUPRAVITAL STAINS
36
explain mature RBC
7-9 micrometer in diameter pink cytoplasm round, biconcave, non-nucleated
37
explain erythropoiesis
initiated by erythropoietin, produced in the KIDNEYS erythropoietin production is stim by HYPOXIA functions - activate stem cells of bone marrow to diff into pronormoblasts - increase rate of mitosis, maturation process, and rate of Hb production - causes increased rate of reticulocyte release into peripheral blood
38
differentiate the types of granulocytes
neutrophils = pink to rose - violet granules eosinophils = reddish orange granules basophils = dark purple granules
39
explain neutrophil differentiation
main cytokine initiating neutrophil production = G-CSF myeloblasts --> promyelocytes --> myelocytes --> metamyelocytes --> bands and segments myeloblasts, promyelocytes, and myelocytes undergo cell division (mitotic pool) metamyelocytes, bands, and segments DO NOT divide (maturation and storage pool) leave storage pool and enter peripheral blood --> 50% circulate freely and 50% adhere to walls of bvs (marginal pool) neutrophils continually move between circulating and marginal pools granules have destructive enzymes (MPO) to destroy infectious orgs have prominent phagocytic activity mature segmented neutrophil granulocytes are known as PMNs
40
explain segmented granulocyte
9-15 micrometer in diameter abundant granules (pink to violet in neutrophils) cytoplasm 2-5 lobes and coarsely condensed chromatin in nucleus
41
explain eosinophil differentiation
similar maturation stages to neutrophils large eosinophilic granules mature have 2 nuclear lobes granules have destructive enzymes to fight organisms that are TOO BIG TO PHAGOCYTOSE (fungi, protozoans, and parasites) also involved in modulation of mast cell activity in HYPERSENSITIVITY/allergic disease minimal degree of phagocytic activity main cytokine initiating eosinophil production = IL-5
42
explain basophil differentiation
mature have prominent, large, dark blue cytoplasmic granules that obscure nucleus multilobar but NON-SEGMENTED nucleus found in blood and marrow at low levels involved in hypersensitivity/allergic processes and innate defenses against microbes main cytokine initiating production = IL-3
43
innate vs adaptive immunity
adaptive immunity = T and B cells innate immunity = NK cells
44
lymphocytes that become very big are called...
transformed, atypical, or viral lymphocytes
45
describe plasma cells
make Abs to specific Ags CLOCK FACE chromatin (boiled egg appearance), eccentric nucleus normal in bone marrow but NOT IN peripheral blood
46
explain monocyte differentiation
12-20 micrometer in diameter abundant BLUE GRAY with many purple granules and frequent VACUOLIZATION variable shaped and very often convoluted nuclear mem initiated by M-CSF mature monocytes circulate in peripheral blood for abt 20 days before entering tissues to become MACROPHAGES some mature monocytes and macrophages reside in marrow
47
explain megakaryocyte differentiation
very large cells with highly folded, MULTILOBILAR NUCLEI, abundant finely granular cytoplasm possess PSEUDOPODS, allow direct shedding of platelets into circulation millions of platelets are produced every sec products can be increased up to 20 fold in response to STRESS production initiated by CYTOKINE THROMBOPOIETIN (TPO) on megakaryocyte/erythroid progenitor cell
48
what are the causes of hypocellular marrow?
autoimmune attack viral attack hematopoietic neoplasms malnourished states
49
what are the causes of hypercellular marrow?
after blood loss (anemia), platelet destruction sepsis chronic myeloproliferative states - chronic myeloid leukemia (CML) - acute leukemia - myelodysplastic syndromes (MDS)
50
dx for myeloblast are...
AUER RODS
51
promyelocytes are...
largest cell in bone marrow after megakaryocytes, contains primary granules
52
describe metamyelocytes
abundant, many specific granules in cytoplasm indented or KIDNEY SHAPED NUCLEUS
53
describe bands
same as metamyelocytes --> abundant, many specific granules in cytoplasm ROD or band shaped, COARSELY CLUMP CHROMATIN
54
what is MCV?
mean corpuscular vol normal is 80-100 fL microcytic = low normocytic = normal macrocytic = high
55
what is RDW?
RBC distribution width normal is 11.5-14.5% abnormal variation in cell VOLUME = anisocytosis abnormal variation in cell SHAPE = poikilocytosis
56
what is MCH?
mean corpuscular Hb represents mean mass of Hb in RBC normal is 28-33 pg
57
what is MCHC?
mean corpuscular Hb concentration concentration of Hb in a given vol of packed RBCs normal is 32-36 g/dL norm = normochromic high = hyperchromic low = hypochromic
58
what are the diseases of spherocytes?
hereditary spherocytosis drug and infeciton-induced immune hemolytic anemia
59
what are the diseases of elliptocytes?
hereditary elliptocytosis
60
what are the diseases of stomatocytosis?
alcholism cirrhossi obstructive liver disease hereditary marathon runners RBC sodium pump defect Rh null disease artifact
61
what are the diseases of macro-ovalocytes?
megaloblastic anemia
62
what are the diseases of target cells?
thalassemia liver disease Hb C
63
what are the diseases of sickle cells?
sickle cell anemia due to LOW O2 conditions like in high alts and acidosis
64
what are heinz bodies present in?
G6PD deficiency (oxidative injury) unstable Hbs (contain iron) SUPRAVITAL stain (crystal violet, methylene blue)
65
what are bite cells present in?
G6PD deficiency due to removal of heinz bodes by splenic macrophages
66
what a schistocytes?
microangiopathic hemolytic anemias - DIC - TTP - HUS - HELLP syndrome - mechanical hemolysis (heart valve hemolysis) see fragmented RBCs, HELMET SHAPE
67
what is HELLP?
hemolysis, elevated liver enzymes, low platelets, severe variant of preeclampsia
68
what are acanthocytes?
spur cells LIVER DISEASE and abetalipoproteinemia
69
what are echinocytes?
echino = prickly burr cells LIVER DISEASE, ESRD, and PKD
70
what are howell jolly bodies present in?
ASPLENIA, MDS removed by splenic macrophages
71
what causes basophilic stippling?
- LEAD poisoning - ARSENIC poisoning - SIDEROBLASTIC ANEMIA - THALASSEMIA - ALCOHOLISM
72
what causes dacrocyctes?
teardrop cells bone marrow infiltration (myelofibrosis) and thalassemia
73
explain the function of neutrophils
most populous and most short lived circulate for about 8 hours before entering tissues for abt a wk normally circulating neutrophils consists of BAND and SEGMENTAL neutrophils LEFT SHIFT IS INDICATOR OF ACUTE STRESS
74
what is leukemoid reaction?
marked leukocytosis with granulocytosis and a granulocyte left shift resembles CML reactive morphology (toxic granules, DOHLE BODIES) HIGH LEUKOCYTE ALKALINE PHOSTPHATASE (high LAP score)
75
what is flow cytometry?
allows for indv measurements of cell fluorescence and light scattering process performed at rates of thousands of cells per sec info can be used to individually sort or separate subpops of cells how it works - Abs recognize specific molecules on surface of some cells (Abs are conjugated to fluorochromes) - when cells are analyzed by flow cytometry, the ones with the marker for which the Ab is specific, will fluoresce - cells lacking marker will not
76
why FSC vs SSC?
FSC looks at size SSC loos at internal structure
77
acute blood loss is due to...
loss of intravas vol which if massive can lead to cardio collapse, shock, and death normocytic normochromic anemia - decreased circulating vol --> shock - compensatory hemodilution (decreased HCT) - increased hematopoiesis, increased reticulocytes (max at 7-10 days) due to trauma
78
chronic blood loss is due to...
GI tract lesions or gynecologic disturbances normocytic normochromic anemia (initially) - often compensated, mild symps - increased reticulocytes due chronic GI, gyn, or GU blood loss
79
what happens when there is hemolysis?
premature destruction of RBCs elevated erythropoietin and comp increase in erythropoiesis accum of Hb degradation products released by red cell breakdown derived from Hb
80
what is intravas hemolysis?
- due to mechanical injury (cardiac valves, marathon runners) - complement fixation - parasites (falciparum malaria) - toxic insults hemoglobinemia (decrease haptoglobin) HEMOGLOBINURIA (JAUNDICE) increased fecal urobilin increased serum LDH schistocytes, increased LDH, decreased haptoglin, increased free Hb and urine Hb, HEMOSIDERINURIA
81
what is extravasc hemolysis?
caused by reduced deformability clinical feats = ANEMIA, SPLENOMEGALY, and JAUNDICE*** increased bilirubin --> jaundice, pigment gallstones increased fecal urobilin decreased haptoglobin increase serum LDH microspherocytes, increased LDH, decrease haptoglobin, increased indirect bilirubin, increase urine and fecal urobilinogen
82
what are the types of intravasc hemolysis?
ABO and Rh incompatibility PNH paroxysmal cold hemoglobinuria snake envenomation infection (malaria, babesiosis, clostridium)
83
what are sideroblasts?
erythroblasts with intracytoplasmic membrane-bound ferritin molecules
84
what is ring sideroblast?
perinuclear granules
85
what is bone marrow lab used for in iron deficiency anemia?
last test indicated used to see if it's a refractory anemia
86
in anemia, reticulocytes are...
falsely elevated reticulocyte index (corrected RC) = reticulocyte % x actual Hct/normal Hct corrected RC count >3% = good marrow response to peripheral destruction corrected RC count <3% poor marrow response (underproduction)
87
what is norm Hct?
45%
88
what are the effects of vit B12 tx?
folate may resolve megaloblastic anemia of B12 deficiency, but has NO EFFECT ON NEURO SYMPS
89
what is the function of hepcidin in iron absorption?
normally iron is transported into the parietal cells through heme transporter --> iron will pass through ferroportin to be absorbed --> when iron levels are high, liver will release hepcidin to inhibit ferroportin from absorbing more iron when levels are low, there is low plasma hepcidin so more iron passes thru ferroportin when levels are high, there is high plasma hepcidin which will destroy ferroportin to inhibit iron absorption
90
on gel, Hb migrates from...
negatively charged cathode to positively charged anode HbA migrates furthest, HbF, HbS, HbC A Fat Santa Clause
91
what is a folic acid antagonist?
methotrexate
92
what are the 2 anemic conditions children?
PKD (newborns) paroxysmal cold hemoglobinuria
93
what are the steps of coagulation short?
vasoconstriction platelet plug (temporary plug) local activation of coagulation system (permanent clot)
94
explain coagulation
vasoconstriction due to release of endothelin, reflex constriction of site of injury primary hemostasis - platelet adhesion to vWF - platelet shape change - granule release - recruitment of more platelets - aggregation and formation of hemostatic plug secondary hemostasis - tissue factor binds to platelets - phospholipid complex expression - thrombin activation - fibrin polymerization thrombus and antithrombotic events - release of t-PA (fibrinolysis) - thrombomodulin (blocks coagulation cascade)
95
what is the function of factor XIII?
stabilizes fibrin clot
96
explain fibrinolysis
plasminogen gets converted into plasmin with the help of tPA, urokinase, and factor XIa and XIIa plasminogen activator inhibitor 1 and 2 inhibit tPA and urokinase plasmin will stimulate fibrin to be cut into fibrin degradation products plasmin is inhibited by a2-antiplasmin and a2-macroglobulin cutting of fibrin is inhibited by thrombin-activatable fibrinolysis inhibitor
97
what is virchow's triad in thrombosis?
endothelial integrity is most important factor injury to endo cells can alter local blood flow and affect coagulability abnormal blood flow can cause endo injury
98
what are platelets?
small discoid cells (cytoplasm w/o nucleus) 2-3 micrometer diameter 7-10 day lifespan contain intracell granules (alpha and theta) that contain coagulation factors and ADP actin, myosin activated platelets form TEMP PLUG 300k platelets/microliters of blood produced in bone marrow from megakaryocytes production stimulated by TPO from liver/kidney main fxn is to stop bleeding from defects in bv walls by forming a plug at site of injury and promote coagulation
99
what factors are on the platelet surface?
IIb-IIIa = after platelet activation binds FIBRINOGEN, necessary for aggregation Ib-IX-V = binds vWF, necessary for platelet adhesion at HIGH shear rates Ia-IIA = binds COLLAGEN mediates adhesion at LOW shear rates and platelet spreading
100
explain platelet adhesion, activation, and aggregation
adhesion - endo damage = exposure of collagen --> vWF --> platelet Ib/V/IX - platelet IA/IIa --> collagen, low shear rate activation = activated platelets release granules (ADP, serotonin) and activate IIb/IIIa aggregation = activated IIb/IIIa --> fibrinogen Bernard Soullier syndrome --> affects ADHESION, vWf, CD42, and Ib/V/IX Glanzmann thrombasthenia --> affects AGGREGATION, FIBRINOGEN, CD41/CD61, IIb/IIIa
101
what are the disorders of platelets?
quantitative - low plts (thrombocytopenia) consumption = TTP, ITP, HIT production = aplastic anemia, chemoradiotherapy - high plts (thrombocytosis) reactive = iron deficiency, acute blood loss, splenectomy clonal (neoplastic) = essential thrombocythemia, AML-M7 familial = rare qualitative - acquired - inherited
102
pxs with low plt counts or fxnal abnormalities of plts may present with...
petechiae, purpura, mucosal hemorrhage, menorrhagia, and prolong bleeding after cuts
103
explain PT
monitor WARFARIN therapy prolonged PT - VII deficiency (extrinsic) - vit K deficiency (1972) - COMMON factor deficiency = increased PT > increased PTT - inhibitor
104
explain aPTT
normal <40 secs monitor HEPARIN therapy measures all factors except VII and XIII prolonged aPTT - heparin - INTRINSIC factor deficiency = XII, XI, IX, VIII - COMMON factor deficiency = X, V, II, I - lupus anticoagulant = PTT better than PT - vit k deficiency = PT is better
105
how do you know if there's a factor deficiency or inhibitor in the blood?
factor deficiency = clotting time CORRECTS when px's plasma is mixed with normal plasma inhibitor = clotting time FAILS TO CORRECT when px plasma is mixed with normal plasma (heparin anticoagulation, acquired inhibitors)
106
what is antithrombin III deficiency?
causes hypercoagulability decreased activity of heparin which is a blood thinner PTT doesn't increase after heparin administration
107
what is factor V leiden?
most common cause of inherited hypercoagulability in caucasians mutant factor V leiden --> resistance to degradation by activated protein C --> DVT, cerebral v thrombosis, recurrent preg loss
108
what happens in protein C or S deficiency?
increased risk of thrombotic skin necrosis with hemorrhage after warfarin administration decreased ability to inactivate factors Va and VIIIa
109
what happens in prothrombin gene mutation?
causes hypercoagulability increase production of prothrombin --> venous clots
110
why are D-dimers important?
they're characteristic of DIC but not specific there are many other causes that lead to elevated D-dimers
111
what are the blood transfusion therapies?
acute blood loss or severe anemia = packed RBCs thrombocytopenia or qualitative plt defects = plts FFP for cirrhosis (immediate anticoag reversal), contains all coag factors and plasma proteins prothrombin complex concentrate (PCC) contains factors II, VII, IX, X, protein C and S (vit K deficiency) cryoprecipitate contains fibrinogen, factors VIII, XIII, vWF, indicated in coag factor deficiencies involving fibrinogen and FVIII
112
what are the transfusion complications?
febrile non-hemolytic rxn = fever and chills within 6 hrs of transfusion of RBCs allergic rxns = most likely IgA deficiency, utricarial rxn iron overload can lead to hemochromatosis hypocalcemia (CITRATE is calcium chelator) hyperkalemia (lysed RBCs in old blood)
113
what are hemolytic rxns?
ACUTE rxns usually caused by pre-formed IgM Abs most commonly due to px misid (ABO mismatch) DIRECT COOMBS TEST IS POSITIVE symps due to complement activation rather intravasc hemolysis
114
delayed hemolytic rxns are caused by...
IgG abs to Ags like RH, Kell, Kidd intensity varies
115
what is TRALI?
within 6 hrs of transfusion, severe dyspnea, fever, chills, cyanosis, hypoxemia, pulm edema, HYPOTENSION, ABSENCE OF OTHER CLINICAL INDICATORS OF FLUID OVERLOAD ab to HLA I, II, granulocyte, monocyte, IgA associated with active infection/sepsis, surgery, severe burn injury, history of cytokine administration
116
what is TACO?
similar presentation to TRALI jugular venous distention HYPERTENSION improvement of symps with diuresis
117
what are the primary vs secondary lymphoid organs/tissues?
primary lymphoid organs - bone marrow = B lymphocytes (CD20+) - thymus = T lymphocytes (CD3+) lymphocytes circulate thru blood and home to... secondary lymphoid tissues - lymph nodes - spleen - tonsils - adenoids - peyer patches
118
what is characteristic of the thymus?
Hassall's corpuscle
119
follicular lymphoma can transform to...
diffuse large B cell lymphoma
120
what is rituximab?
chimeric monoclonal Ab against CD20, which is found on surface of B cells --> so it destroys the B cells
121
what is characteristic of multiple myeloma?
CRAB M spikes lytic, punched out bone lesions Rouleaux formation only see IgG on serum with kappa light chain
122
what is characteristic of Burkitt lymphoma?
starry sky histo
123
what is characteristic of CLL/SLL?
smudged cells on histo
124
what is characteristic of Classic Hodgkin lymphoma?
Reed Sternberg cells (owl eyes)
125
what is characteristic of nodular lymphocyte predom Hodgkin lymphoma?
L&H cells aka POPCORN CELLS
126
what are the myeloid neoplasms?
acute myeloid leukemia MDS chronic myeloproliferative neoplasms
127
what are the lymphoid neoplasms?
precursors B and T cell neoplasms mature B and T cell neoplasms Hodgkin lymphoma
128
what are the mature T cell neoplasms?
- peripheral T cell lymphoma - angioimmunoblastic T cell lymphoma - adult T cell leukemia/lymphoma - anaplastic T cell lymphoma - mycosis fundoides/sezary syndrome - large granular lymphocytic leukemia - extranodal NK/T cell lymphoma
129
what is characteristic of hairy cell leukemia?
boil egg appearance of cells
130
what are the conditions that have lytic bone lesions?
multiple myeloma adult T cell lymphoma/leukemia Langerhans cell histiocytosis
131
what is characteristic of adult T cell lymphoma/leukemia?
skin lesions, lytic bone lesions FLOWER CELLS
132
what is characteristic of sezary syndrome?
cerebriform nuclei
133
B cell vs T cell lymphoblastic leukemia/lymphoma
B cell more common in CHILDHOOD (as leukemia) T cell more common in ADOLESCENTS (as lymphoma) B-cell ALL is most common malig of childhood
134
what are the disorders of the spleen and thymus?
splenomegaly thymic hyperplasia thymoma thymic carcinoma
135
what conditions have splenomegaly?
spleen >1000g chronic myeloid leukemia primary myelofibrosis CLL hairy cell leukemia many lymphomas (B and T)
136
what is the only condition w/o lymphadenopathy?
mycosis fungoides/sezary syndrome (CD4+, CD3+, CD7-)
137
what is characteristic of MDS?
pseudo pelger huet cell hypolobate and hypogranular
138
what defines MDS?
deletion of 5q defines MDS subtype
139
auer rods are specific for...
myeloblasts when seen in MDS on PBS or BM, dx = MDS if there are <20%
140
what are the AMLs that do not require 20% blasts for dx?
AML with t(8,21) AML with 1(16,16) or inv(16) AML with t(15,17)
141
AML is associated with...
life threatening DIC auer rods
142
what is imatinib?
first tyrosine kinase inhibitor blocks binding of ATP to the BCR tyrosine kinase, inhibiting its activity
143
what is seen in the PBS of CML in chronic phase?
prominence of myelocytes and segmented neutrophils basophils are invariable increased in absolute numbers
144
bone marrow in CML chronic phase is...
HYPERCELLULAR
145
what is seen in the bone marrow of CML in blast phase?
sheets of blasts with some eosinophils intermixed contains abnorm blasts with t(9,22)
146
explain PV based on the WHO criteria
2 major + 1 minor of 2 minor + 1 major major - HgB >18.5 in men and 16.5 in women - JAK2 mut minor - bone marrow panmyelosis - endogenous erythroid colony formation in vitro - NORMAL SERUM EPO JAK2 mut, 95% cases, mostly V617F cause of death = thrombosis 31%, acute leukemia 19%
147
explain ET based on WHO criteria
sustained thromcytosis >450x10^9/L bone marrow shoes megakaryocytic HYPERPLASIA, w/o panmyelosis fails to meet criteria for PV, PMF, CML, or MDS JAK2 mut neg criteria - exclude other myeloprolifs (NO BCR/ABL rearrangement) - exclude secondary thrombocytosis splenomegaly JAK2 mut in 50% of cases clinically = bleeding or thrombosis good prognosis
148
what do you see in PBS of ET?
largely unremarkable, except for THROMBOCYTOSIS (800x10^9) bone marrow has norm cellularity but INCREASED numbers of large megakaryocytes with HYPERLOBULATED nuclei
149
what do you see in PBS of the 2 phases of PMF?
prefibrotic - neutrophilia and thrombocytosis - minimal red cell changes - mimicking ET fibrotic - leukoerythroblastosis - marked red cell abnorms - many TEAR DROP cells - circulating nRBCs also use reticulin stain
150
what is characteristic of primary myelofibrosis?
dacrocytes
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