FA: Heme Onc Flashcards
1
Q
how long do RBCs live?
A
120 days
2
Q
what do RBCs use for energy
A
glucose. 90% glycolysis and 10% from HMP shunt
3
Q
important membrane antiporter in RBCs
A
HCO3- antiporter which allows RBCs to export HCO3- and transport Co2 from the periphery to the lungs for elimination
4
Q
erythrocytosis
A
too many red blood cells
5
Q
anisocytosis
A
variation in size of RBCs
6
Q
Poikilocytosis
A
varying shapes of RBCs
7
Q
reticulocyte
A
immature RBC, marker of erythroid proliferation
8
Q
lifespan of platelet
A
8-10 days
9
Q
job of platelets
A
primary hemostasis
10
Q
dense granules in platelets contain
A
ADP and calclium
11
Q
alpha granules in platelets contain
A
Von Willibrand Factor and fibrinogen
12
Q
thrombocytopenia
A
low platelet level. this or decreased platelet function results in petechiae
13
Q
which receptor on platelet attaches to VWF
A
GpIb
14
Q
which receptor on the platelet attaches to fibrinogen
A
GP2b/3a
15
Q
what are three granulocytes
A
neutrophils, eosinophils and basophils
16
Q
normal WBC
A
4,000-10,000
17
Q
pneumonic for WBC differential
A
Neutrophils Love Making Everyone Better Neutrophils Lymphocytes Monocytes Eosinophils Basophils
18
Q
normal percentage of Neutrophils
A
54-62%
19
Q
normal percentage of Lymphocytes
A
25-33
20
Q
normal percentage of monocytes
A
3-7
21
Q
normal percentage of eosinophils
A
1-3
22
Q
normal percentage of basophils
A
0-1
23
Q
cell with a multi lobed nucleus
A
this is a neutrophil
24
Q
specific granules of neutrophils
A
contain ALP, collagenase, lysozyme, and lactoferrin
25
azurophilic granules of neutrophils
contain proteinases, acid phosphatase, myeloperoxidase, and beta glucoronidase
26
hypersegmented polys
this is a neutrophil with more than 5 lobes. seen in vitamin B12 and folate deficiency
27
band cell
immature neutrophil
28
when do you see increased band cells
infections (bacterial) and CML
29
Monocyte appearance on histology
kidney shaped nucleus. blue. frosted glass cytoplasm
30
function of a monocyte
differentiates into macrophages in the tissues
31
what activates macrophages
gamma interferon
32
macrophages are antigen presenting cells with MHC type...
MHC type II
33
what is the cell surface marker for macrophages
CD14
34
function of eosinohpil
anti helminthic infections.. highly phagocytic for antigen-antibody complexes
35
how do eosinophils fight off helminths
major basic protein.
36
how to recognize eos
bi-lobed nucleus
37
two things produced by eosinophils
histaminase and arylsulfatase. limit reaction during mast cell degranulation.
38
function of basophils
allergic reactions.
39
contents of basophil granules
basophilic granules with heparin, histamine and leukotrienes.
40
if you see isolated basophilia what should you worry about?
CML
41
mast cell function
mediates allergic reactions. can bind to the Fc portion of IgE to membrane and cause IgE cross linking.
42
what does degranulation of mast cells release
histamine, heparin, and eosinophil chemotactactic factors
43
what prevents mast cell degranulation
cromolyn sodium
44
function of denritic cell
antigen presenting cell, high phagocytic
45
what type of MHC does dendritic cell have
MHC type II and Fc receptor on surface.
46
what do we call dendritic cells in the skin
Langerhans cells
47
Three types of lymphocytes
B cells, T cells and NK cells
48
what type of immunity are NK cells part of
innate immunity
49
where do B cells get made
stem cells in bone marrow
50
where do B cells mature
bone marrow
51
which part of lymph node can B cells be found in?
follicle and white pulp of spleen
52
cell of humoral immunity
B cell
53
cell of cellular immunity
T cell
54
where do T cells mature
thymus gland
55
CD8 T cells
cytotoxic T cells- express CD8 and recognizing MHC 1
56
CD4 T cells
helper T cells, express CD4 and recognize MHC2
57
CD28 marker
this is for regulatory T cells which is a costimulatory signal necessary for T cell activation
58
what cell is effected in multiple myeloma
plasma cell disease
59
do anti A and anti B IgM antibodies cross the placenta
NO
60
do anti Rho IgG cross the placenta
Yes
61
universal recipient of RBCs
AB
62
universal donor of RBCs
O
63
universal donor of plasma
AB (these people's plasma have no antibodies in it)
64
universal recipient of plasma
O (because they have A and B antibodies already in their plasma)
65
hemophilia A has a deficiency in
factor 8
66
hemophilia B has a deficiency in
factor 9
67
factor 2
prothrombin
68
factor 2a
thrombin
69
what does kalikrein activate
bradykinin
70
what is the function of bradykinin
increase vasodilation, permeability and pain.
71
famous enzyme that inactivates bradykinin
ACE. hence why ACE inhibitors cause cough
72
what enzyme does warfarin inhibit
epoxide reductase which reduces vitamin K so it can be used as an activator of the factors 2,7,9,10
73
what activates protein C
thrombin thrombomodulin complex in the endothelial cells
74
what activates plasminogen
tpa
75
what is the function of protein C and protein S
cleave and inactive factor 5 and 8
76
function of antithrombin III
inhibits activated forms of factor 2, 7,9,10, 11, 12
77
how does heparin work
it increases the activity of antithrombin III
78
what are the major targets of antithrombin
factor 2 (thrombin) and factor 10a
79
what does plasmin do
responsible for fibriolysis. cleaves the fibrin mesh and destorys the coagulation factors. it is activated by tpa
80
factor V leiden mutation
this produces a factor 5 that is not sensitive to the work of protein C
81
thing that helps with platelet adhesion
VMF
82
thing that helps with platelet aggregation
ADP which induces Gp2b/3a and TXA2 which attracts more platelets which causes fibrinogen to be able to attach and cause aggregation
83
how does aspirin prevent the clot from forming
prevents TXA2 production so you do not attract the platelets to the area for aggregation
84
Ticlopidine and Clopidogrel mechanism
inhibit ADP induced G2b/3a expression so you can't form the clot. basically blocks the ADP receptor so it can't be activated
85
abciximab mechanism
inhibits g2b/3a directly
86
ristocetin mechanism
activates vMF to bind Gp1b. used for diagnostic test- if there is vWF disease, normal platelet aggregation is not seen.
87
Bernard Soulier syndrome
deficiency in Gp1b
88
Glanzmann thrombasthenia
deficiency in Gp2b/3a
89
what is the SED rate
increase in fibrinogen which is an acute phase reactant so the RBCs aggregate more causing them to settle more because RBC aggregates have a higher density than plasma.
90
low SED rate?
polycythemia, sickle cell anemia, CHP, microcytosis, hypofibrinogenemia
91
acanthocyte (spur cell) of the RBC
liver disease, abetalipoproteinemia- cholesterol dysregulation
92
basophilic stippling of the RBC
microcytic anemias- anemia of chronic disease, alcohol, lead poisoning and thalassemias (not iron def)
93
bite cell
G6PD deficiency
94
Elliptocyte
RBC showing hereditary elliptocytosis
95
macro-ovalocyte
megaloblastic anemia and marrow failure
96
hypersegmented PMN
megaloblastic anemia
97
ringed sideroblast
sideroblastic anemia - defect in heme production
98
schistocyte or helmet cell
DIC, TTP, HUS, traumatic hemolysis like with mechanical valve prosthesis
99
sickle cell
sickle cell anemia
100
spherocyte
hereditary spherocytosis- spectrin mutation. also seen in autoimmune hemolysis
101
teardrop cell
bone marrow infiltration like myelofibrosis.
102
target cell
Hemoglobin C disease, asplenia, liver disease, thalassemia
103
Heinz Bodies
this is from oxidation of hemoglobin sulhydryl groups- denatured hemoglobin precipitates and phagocytic damage to RBC leads to bite cells. visualized with crystal violet. seen in G6PD
104
Heinz body like inclusions
these can be seen in alpha thalassemia from the precipitated hemoglobin
105
howell jolly bodies mechanism
basophilic nuclear remnants found in RBCs that would have normally been removed by the spleen. seen in patients with functional hyposplenia and asplenia
106
other causes of megaloblastic anemia aside from B12 and folate deficiency
orotic aciduria.
107
type of anemia with iron deficiency anemia
microcytosis and hypochromia
108
plummer vinson syndrome
triad of iron deficiency anemia, esophageal webs, and atrophic glossitis
109
cis alpha thal deletion population
asian population
110
trans alpha thal deletions
present in African populations
111
hemoglobin barts
gamma x4. incompatible with life
112
4 allele deletion in alpha thal
incompatible with life. hemoglobin barts. causes hydrops fetalis
113
3 allele deletion in apha thal
hemoglobin H. excess beta joins together and you get Beta 4 which is hemoglobin H
114
1-2 allele deletion in alpha thal
not clinically significant
115
alpha thal... what is the issue
this is a deletion in the alpha globin gene
116
beta thal.. what is the issue
this is a mutation in the splice sites which reduces beta thal synthesis.
117
population where you see beta thal
Mediterranean populations
118
Beta thal minor
heterozygote. beta chain is underproduced. usually asymptomatic. diagnosis is confirmed with increased HA2 on electorphoresis (>3.5%)
119
beta thal major
beta chain is absent leading to severe anemia. requires blood transfusions which can give secondary hemochromatosis.
120
classic deformity seen with beta thal major
extramedullary hematopoiesis leads to hepatosplenomgaly. increased risk of parvo virus aplastic crisis. marrow expansion shows crew cut on skull x ray and chipmunk face.
121
how does lead poisoning cause anemia
inhibits ferochelatase and ALA dehydrogenase. this decreases heme synthesis and increases RBC protoporphyrin. also inhibits rRNA degradation causing RBCs to retain aggregates of rRNA (basophilic stipling).
122
burton lines
these are lead lines on gingivae and also seen in metaphysis of bones.
123
first line treatment of lead poisoning
dimercaprol and EDTA . can also use succimer for chelation for kids.
124
sideroblastic anemia
defect in heme synthesis
125
mutation for hereditary sideroblastic anemia
X linked defect- delta- ALA synthase gene mutation.
126
reversible causes of sideroblastic anemia
ALCOHOL, lead, B6 deficiency, copper deficiency and isoniazid
127
treatment for sideroblastic anemia
B6 (pyroxidine)
128
labs in sideroblastic anemia
increased iron, normal TIBC, increased feritin.
129
what does the term megaloblastic anemia mean
this means there is impaired DNA synthesis. maturation of the cells in the bone marrow is delayed relative to maturation of cytoplasm.
130
what test to distinsguish between folate and B12 deficiency
MMA
131
3 drugs that cause folate deficiency and megaloblastic anemia
methotrexate, trimethoprim, phenytoin.
132
should there be any neurologic symptoms in folate deficiency?
no because these symptoms are from the B12 deficiency and its role in fatty acid pathways and myelin synthesis
133
what bug likes to eat B12
diphyllobothrium latum which is a fish tapeworm
134
hypersegmented neutrophils, glossitis and orotic acid in urine
orotic aciduria. inability to convert orotic acid to UMP for the denovo pyrimidine synthesis.
135
defect in orotic aciduria
UMP synthase
136
how to distinguish orotic aciduria from ornithine transcarbamylase deficiency
both have increased orotic acid in the urine but orotic aciduria does NOT have increased ammonia.
137
how to treat orotic aciduria
uridine monophosphate to bypass mutated enzyme
138
what is a non megaloblastic macrocytic anemia
this is an anemia in which DNA synthesis is not impaired. causes include liver disease, alcoholism, reticulocytosis, drugs (5FU, zidovudine, hydroxyurea)
139
if you see decreased haptoglobin
think intravascular hemolysis with normocytic anemia
140
causes of intravascular hemolysis with normocytic anemia
paroxsymal noctural hemoglobinuria, mechanical destruction, microangiopathic hemolytic anemia
141
extravascular hemolysis findings
spherocytes, increased LDH, increased unconjugated bilirubin, jaundice
142
cause of extravascular hemolysis
hereditary spherocytosis
143
what type of hemolysis shows increased urobilinogen in urine?
intravascular because this is conjugated.
144
fatty infiltration of the bone marrow
aplastic anemia
145
causes of G6PD crisis
sulfa drugs, antimalarials, infections, fava beans
146
lab findings of Heinz bodies and bite cells
G6PD deficiency
147
hemolytic anemia in a newborn
pyruvate kinase deficiency. decrease in ATP leads to a firm or rigid RBC
148
defect in HgC defect
glutamic acid to lysine mutation on residue 6 of Beta globin
149
mutation in paroxysmal nocturnal hemoglobinuria
impaired synthesis of GPI anchor for decay accelerating factor that protects RBCs form complement destruction. intravascular hemolysis
150
labs to diagnose paroxysmal nocturnal hemoglobinuria
CD55 and CD59 negative RBCs. coombs negative
151
treatment for paroxysmal nocturnal hemoglobinuria
eculizumab
152
mutation in sickle cell anemia
B chain mutation- has valine instead of glutamic acid
153
what precipitates sickling
low O2, dehydration, acidosis.
154
crew cut on Xray
you can see this here and with the thalassemias
155
type of osteomyelitis seen in sickle cell
salmonella
156
most common cause of death from sickle cell
acute chest syndrome
157
treatemtn for sickel cell
hydroxyurea to increase the hemologbin F. bone marrow transplantation also
158
coombs test is positive in what disease
autoimmune hemolytic anemia
159
warm agglutinin
IgG chronic anemia seen in SLE, CLL, or with drugs like alpha methyldopa
160
cold agglutinin
IgM acute anemia triggered by cold. seen in CLL, mycoplasma pneumonia, infections like mono
161
direct coombs test
put anti Ig antibody into the patient's serum and see if the red blood cells are coated with Immunoglobuin.
162
indirect coombs test
take the patient's serum and add normal RBCs. see if they clump together or agglutinate.
163
microangiopathic hemolytic anemia mechanism
RBCs are damaged when passing through obstructed or narrowed vessel lumina. seen in DIC, HUS, TTP, SLE
164
what is classic finding in microangiopathic hemolytic anemia
schistocytes or helpmet cells
165
what diseases are associated with microangiopathic anemia?
prosthetic heart valves and aortic stenosis
166
pregnancy and lab values for iron tests
increased TIBC and decreased saturation of iron. all else is the same.
167
Neutropenia
absolute neutrophil count of <1500
168
lymphopenia
absolute lymphocyte count <1500
169
eosinopenia
cushing syndrome, corticosteroids.
170
corticosteroids and white count
corticoisteriods cause neutrophilia, but eosinopenia, and lymphopena.
171
how do corticosteroids increase neutrophil count
they do this by decreasing the activation of neutrophil adhesion molecules so they cannot migrate out of the vasculature and into the tissue.
172
how do corticosteroids decrease lymphocytes and eosinophils
steroids sequester eosinophils in the lymph nodes and cause apoptosis of lymphocytes
173
what is a porphyria
this is a hereditary or acquired defect in heme synthesis that leads to the accumulation of heme precursors.
174
how does lead posioning affect heme
can't produce heme. affects two enzymes- ferochelatase which adds the Fe to the Heme. it also causes a problem with the enzyme delta ALA deaminase
175
what is the mutation in a sideroblastic anemia (X linked)
mutation in the first enzyme in heme production which is the rate limiting step- this is delta ALA synthase.
176
what substrates accumulate in lead poisoning
protophorphyrin and delta ALA. it cannot turn the delta ALA into porphobilinogen.
177
which step in heme production requires B6
the first (rate limiting) step requires B6. this is the conversion of glycine and succinyl CoA into delta ALA. the enzyme that does this is ALA synthatase
178
which adults would get lead poisoning
battery/ammunition/radiator factory. headache, memory loss and demylination.
179
enzyme mutation in acute intermittent porphyria
porphobilinogen deaminase
180
what builds up in acute intermittent porphyria
porphobilinogen, delta ALA, coporphobilinogen in the urine
181
symptoms of acute intermittent porphyria
painful abdomen, port wine colored urine, poyneuropathy, psychological disturances, precipitated by drugs, alcohol and starvation
182
treatment of acute intermittent porphyria
glucose and heme. heme inhibits ALA synthetase
183
porphyria cutanea tarda symptoms
blistering cutaneous lesions that are photosensitive. most common porphyria.
184
enzyme deficient in porphyria cutanea tarda
uroporphyrinogen decarboxylase
185
what builds up in porphyria cutanea tarda
uroporphyrin leading to tea colored urine.
186
what diagnostic test would show hemophilia
PTT
187
hemophilia A defect
factor 8
188
hemophilia B defect
factor 9
189
what lab tests show bleeding problem from vitamin K deficiency
increased PT PTT
190
what test shows platelet problem
bleeding time
191
beranard soulier syndrome
defect in platelet plug formation. decrease in Gp1b so you cannot attach the platelets to VMF. get a decrease in platelet count with this
192
Glanzmann thrombasthenia
increase in bleeding time but normal platelet count. decrease in Gp2b/3a- can't get platelet-platelet aggregation. blood smear shows NO platelet clumping
193
immune thrombocytopenia
anti gp2b/3a antibodies produced. splenic macrophage consumes them. decreased platelet survival. may be triggered by viral illness. labs show increased megakaryocyte count.
194
TTP
thrombotic thrombocytopenic purpura
195
TTP mechanism
inhibition or deficiency of ADAMTS13 (vMF metalloprotease) which leads to a decrease in degradation of VMF multimers. large multimers are around- the platelets increase adhesion and aggregation and you get thrombosis. decreased platelet survival.
196
renal symptoms, fever, neurological symptoms, thrombocytopenia, and microangiopathic hemolytic uremia
these are symptoms of TTP
197
von Willebrand disease
problem with both primary platelet plug formation and the intrinsic coagulation cascade
198
what lab values are increase in von Willebrand disease
definiteily bleeding time but also potentially PTT because of its association with factor 8
199
vWF and factor 8
vWF serves to carry or protect factor 8
200
most common inherited bleeding disorder
vWF diseae
201
ristocetin cofactor assay
used to diagnose vWF. add this with the patients blood and you will get no agglutination because the ristocetin is an antibiotic that causes the Gp1b to come out and the blood to clump. this only happens with vWF around.
202
treatment for vWF disease
DDAVP- releases vWF stored in endothelium
203
what is DIC
widespread activation of clotting leads to a deficiency in clotting factors which creates a bleeding state
204
lab findings in DIC
schistocytes, increased fibrin split products, decreased fibrinogen, decreased factor 5 and 8
205
most common cause of inherited hypercoagulopathy in whites
Factor V Leiden disease
206
how do you find antithrombin deficiency
give heparin and see no change in PTT. on its own it won't cause an issue with the PTT.
207
acquired forms of antithrombin deficiency
can be lost in the urine- renal failure and nephrotic syndrome.
208
what deficiency increases the risk of thrombotic skin necrosis with hemorrage after warfarin
protein c and s deficiency. mostly protein C deficiency though for skin and other tissue necrosis.
209
when to give packed RBCs
acute blood loss, severe anemia
210
when to give platelets
stop significant bleeding from thrombocytopenia
211
when to give fresh frozen plasma
DIC, cirrhosis, wardarin overdose, exchage transfusion in TTP/HUS
212
when to give cryoprecipitate
treat coagulation factor deficiencies involving fibrinogen and factor 8
213
what does cryoprecipitate contain
fibrinogen, factor 8, factor 13, vWF, and fibronectin
214
potential side effects from blood transfusion
hyperkalemia, hypocalcemia, and iron overload
215
leukemia
lymphoic or myeloid neoplasm with involvement of the bone marrow. tumor cells found in peripheral blood
216
lymphoma
discrete tumor mass arising from lymph nodes.
217
leukemoid reaction
inflammatory reaction to infection. increased WBC with increase PMNs. increased ALP etc.
218
diagnosis with reed sternberg cells
Hodgkin lymphoma
219
reed sternberg cell markers
CD15 and CD30. two nuclei often- two eyes- owl eye cells
220
which form of hodgkin lymphoma is most common
nodular sclerosing type.
221
which form of hodgkin lymphoma is best prognosis
lymphocyte rich kind
222
which form of hodgkin lymphoma has worst prognosis
lymphocyte mixed or lymphocyte depleted form
223
8;14 translocation
burkitt lymphoma
224
chromosome 14?
Ig heavy chain
225
chromosome 8?
myc gene (cmyc specifically here)
226
most common form of non hodgkin lymphoma in adults
diffuse large b cell lymphoma
227
14;18 translocation
diffuse large b cell lymphoma and follicular lymphoma
228
11;14 translocation
mantle cell lymphoma
229
chromosome 11?
cyclin -d
230
chromosome 14?
IG heavy chain
231
cell marker for mantle cell lymphoma
CD5
232
chromsome 18?
bcl2
233
painless waxing and waning of lymphadenopathy
follicular lymphoma
234
HTLV1 infection
assocaited with IV drug use. causes adult T cell lymphoma.
235
lytic bone lesions with hypercalcemia in Japanese person, West Africa or Carribean descent
think about adult T cell lymphoma
236
cell marker for mycosis fungiodes and Sezary syndrome
CD4+
237
most common primary tumor arising in the bone in those > 40 yrs
multiple myeloma
238
bence joines protein
immunoglobulin light chain in urine in multiple myeloma
239
rouleaux formation
this is RBCs stacked like poker chips in multiple myeloma
240
if M spike is IgM and no lytic bone lesions
think about Waldestrom macroglobulinemia
241
which immunoglobulin mostly elevated in multiple myeloma
IgG and IgA
242
multiple myelomas disorders assocaited with it
primary amyloidosis
243
myelodisplastic syndrome
stem cell problem with ineffective hematopoiesis.
244
pseudo pelger huet anomaly
neutrophils with bi-lobed nuclei - two nuclear mases with a thin filament of chromatin- that is commonly seen after chemotherapy
245
leukemia
unregulated growth of leukocytes in bone marow.
246
cancer that can present as a mediastinal mass
ALL.
247
age group of ALL
<15 yrs
248
leukemia assocaited with down's syndrome
ALL
249
12;21 translocation
type of ALL with a better prognosis
250
TdT+ marker and CD10+
TdT is a marker of pre T and B cells and CD10 is pre B cells only. seen in ALL
251
what is another name for small lymphocytic lymphoma
CLL
252
ages of CLL
>60yrs
253
B cell markers seen in CLL
CD5+ and CD20+
254
smudge cells in blood smear
CLL
255
what cell is the issue in hairy cell leukemia
B cells
256
TRAP stain
used for hairy cell leukemia
257
dry tap on aspiration
think about hairy cell leukemia causes marrow fibrosis.
258
treatment of hairy cell leukemia
cladribine (2CDA) which is an adenosine analog- inhibits adenosine deaminase
259
disease with auer rods
AML
260
down syndrome
AML can also be seen in down synrome (as with ALL)
261
15;17 translocation
M3 type of AML which is often called acute promyelocytic leukemia.
262
treatment of M3 type AML
all trans retinoic acid (vitamin A) leading to differentiation of myeloblasts.
263
common presentation of M3 type of AML
DIC
264
9;22 chromosome translocation
this is the philadelphia chromosome- CML.
265
chromosome 9 is ...
bcr
266
chromosome 22 is..
abl
267
disease with increased neutrophils, metamyelocytes and basophils
CML
268
disease with very low leukocyte alkaline phosphatase
CML
269
how to differentiate CML from leukemoid reaction?
leukemooid: incr. LAP
CML: decr. LAP
270
treatment for CML
imatinib
271
lytic bone lesions in a child with skin rash or recurrent otitis media with a mass involving the mastoid bone
could be langerhans cell histiocytosis
272
what is langerhans cell histiocytosis
proliferative disorders of dendritic cells
273
cell marker for langerhand cell histiocytosis
S100 and CD1a
274
what type of ganules are seen in langerhan cells
birbeck or tennis racket granules
275
mutation often seen in myeloproliferative disorders
Jak2 growth signaling problem.
276
polycythemia vera
crit >55%. non hereditary mutation in Jak2 gene.
277
patients who are very itchy after their shower
polycythema vera
278
symptoms of erythromelagia
this is severe burning pain and reddish or bluish discoloration due to episodic blood clots in the vessels of the extremities. sign of polycythemia vera
279
cause of secondary polycythemia vera
EPO increase
280
essential thrombocytosis
increase in the number of platelets. bone marrow contains thse shuge megakaryocytes
281
myelofibrosis
fibrotic obliteration of bone marrow with tear drop cells (RBCs) and immature form of myeloid line.
282
which is the one myeloprolfierative disorder that does not have a JAK2 mutation
CML
283
what is relative polycythemia
this is just a decrease in plasma volume. like from dehydration and burns. makes it look like a high crit.
284
what is appropriate absolute polycythemia
this is when you would expect the body to make more RBCs. for example, lung disease, congenital heart disease, high altitude- when its hypoxic. increase in RBC mass and increase in EPO levels to do this and decrease in oxygen saturation
285
inappropriate absolute polycythemia
no change in O2 saturation. this is when you have something making EPO like a renal cell carcinoma, wilms tumor, cyst, hepatocellular carcinoma, hydronephrosis. its all about ectopic EPO. no hypoxia
286
what does a renal cell carcinoma produce
EPO
287
what would EPO levels be like in polycythemia vera
decrease (negative feedback).
288
what would plasma volume and RBC count be in polycythemia vera
increase plasma volume but BIG increase in RBC count
289
why does warfarin cause skin necrosis
from removal of protein C (it inhibits this too)
