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154 Cards in this Set
- Front
- Back
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Myeloblasts have what 3 lineages and what 6 stages
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Neutrophil, eosinophil, basophil
1. promyeloblast 2. promyelocyte 3. myelocyte 4. metamyelocyte 5. stab cell (band cell) 6. final cell |
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do monocytes develop from myeloblasts?
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no, develop form myeloid stem cells, but develop from monoblasts
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WBC cell type differential based on highest to lowest concentration of cells:
eosinophils, neutrophils, basophils, monocytes, lymphocytes |
neutrophils
lymphocytes monocytes eosinophils basophils |
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erythrocyte:
glucose is energy source, 90% derived from what process, 10% from what process? |
90% from anaerobic respiration (produce lactate)
10% from HMP shunt |
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RBCs have what antiport for CO2 transportation?
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cloride-bicarb antiporter
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anisocytosis
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RBCs of varying sizes
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poikilocytosis
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varying shapes
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dense granule contents in platelets (2)
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ADP, collagen (released for platelet aggregation)
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alpha granule contents in platelets (2)
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vWF, fibrinogen (binding agents for platelets)
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what is fibrinogen receptor?
vWF receptor? |
fibrinogen = gp IIb/IIIa
(plavix targets fibrinogen receptor) vWF- gp Ib |
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life span of RBCs?
platelets? |
RBCs - 120 days
platelets - 8-10 days |
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PMN azurophile granules are what and contain what 4 substances
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lysosomes (hydrolytic enzymes, lysozyme, lactoferrin, myeloperoxidase)
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what type of leukocyte has "frosted glass" cytoplasm and kidney-shaped nucleus?
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monocyte (differentiates into macrophage in tissues)
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Macrophages activated by what cytokine? act as APCs via what MHC?
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interferon gamma
MHC class II |
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Eosinophils highly acidphilic for what complexes?
produce what two substances to limit mast cell degranulation reaction? |
antigen-antibody complexes
histiminases, arylsulfatases |
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5 situations that cause eosinophilia
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Neoplasms
Asthma Allergic reactions Collagen Vascular Diseases Parasites |
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basophil mediates what type of rxn?
3 contents of basophilic granules |
allergic reactions (with mast cells)
heparin histimine Leukotrienes (LTD-4) |
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Mast cell:
2 substances released serum marker drug that inhibits release |
substances released : heparin and histimine (like basophils)
serum marker - tyrpase drug that inhibits- cromolyn sodium |
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what are main inducers of primary antibody response, and two protein receptors found on surface
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Dendritic cells
MHC class 2, Fc receptor |
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B cell development:
develop where? once developed, go to what part of: -lymph node -spleen |
develop in marrow
lymph node = follicle spleen = white pulp also found in unencapulated lymphoid tissue (ex. Peyer's patches) |
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T cells originate from stem cells where? develop where?
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originate from stem cells in bone marrow but develop in thymus
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majority of circulating lymphocytes are:
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T cells (80%)
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T cell positive selection (t cell recognition) occurs where? negative T cell selection (not reacting to self) occurs where?
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positive occurs in thymus cortex, negative in thymus medulla
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what type of antibodies are anti-AB antibodies?
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IgM (don't cross placenta)
but anti-Rh are IgG and do cross placenta |
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when is rhogam delivered
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during mother first delivery (because mothers usually exposed to baby Rh during birth)
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plasmin activates what 2 processes?
activated by what what (from plasminogen) |
plasmin activates breakdown of fibrin (clots)
activates complement cascade by activating C3--> C3a activated by Kallikrein (which is activated by factor XIIa) |
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Extrinsic Pathway begins with what factor?
monitored by what measurement and inhibited by what drug? |
Extrinsic pathway
Factor VII PT Warfarin (inhibits II, VII, IX, X, proteins C and S) |
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Intrinsic Pathway begins with what factor?
monitored by what measurement and inhibited by what drug? |
Intrinsic pathway
Factor XII (and XI, IX, VIII) monitored by PTT Heparin (activates antithrombin--> inactivates factors IIa, IXa, Xa, XIa, XIIa) |
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Hemophilia A deficiency?
what measurement(s) will be elevated? inheritance? |
Factor VIII (Intrinsic Pathway component)
PTT x-linked recessive |
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Hemophilia B deficiency?
what measurement(s) will be elevated? inheritance? |
Factor XI (Intrinsic Pathway component)
PTT x-linked recessive |
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Warfarin inhibits what enzyme?
why can neonates present like on warfarin? |
epoxide reductase
because neonates lack enteric bacteria that produce vitamin K |
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vWF carries what factor
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VIII
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Protein C function, 1 mutation against it
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activated by protein S and thrombomodulin (on endothelial cells) to inactivate Factors Va, VIIIa (anticoagulant)
Factor V leiden resistant to Protein C degredation |
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2 factors that activate plasminogen--> plasmin
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kallikrein (activates pathway)
tPA (directly) |
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platelets bind to what at site of vascular injury and binding induces release of what 3 substances?
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platelets bind to vWF, binding induces platelet release of:
-ADP (promotes platelet adherence to endothelium, induces gpIIb/IIIa receptor expression) -Ca2+ (for coagulation cascade) -Thromboxane A2 (increased platelet aggregation and dec. blood flow) |
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2 substances released by endothelial cells that inhibit platelet plug formation
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PGI2, NO
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2 actions of ADP after being released by activated platelets
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1. helps platelets adhere to endothelium
2. activates platelet expression of gpIIb/IIIa |
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Bernard-Soulier syndrome
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deficiency of gpIb (binding of vWF to platelet on damaged surface)
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2 procoagulant substances stored in endothelial cells, 2 anticoagulant substances
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procoagulant - vWF (also found in platelets and on damaged subendothelial collagen), thromboplastin (helps activate thrombin)
anticoagulative substances - tPA, PGI2 |
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syndrome that can manifest from iron-deficient anemia
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Plummer-Vinson syndrome (iron deficienct anemia, atrophic glossitis, esophageal webs
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alpha thalassemia types and associated mutations
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Barts - gamma 4 - hydrops fetalis and incompatible with life
HbH - beta 4 - thalassemia 1 and 2 deletions asymptomatic |
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alpha thalassemia gene mutations in what?
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in alpha-globin genes, resulting in decreased alpha subunit synthesis
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beta thalassemia gene mutations in what?
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point promoter and splicing regions (not in introns!)
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beta thalassemia minor:
what is defect? presentation? |
defect- heterozygote for beta globin mutation
presentation- usually asymptomatic |
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increase of HbA2 over 3.5% on electrophoresis diagnostic of what condition?
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beta thalassemia minor (heterozygous)
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increased HbF seen in what conditions? (3)
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both beta thalassemia minor and major, in sickle cell kids in infancy
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what is common secondary problem in beta thalassemia major?
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2ndary hemochromatosis from repeated transfusions
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"crew cut" skull and chipmunk facies indicate what
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beta thalassemia major (homozygous)
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alpha thalassemia seen in what populations (2)
vs beta thalassemia |
Alpha thalassemia - Asia and Africa
Beta thalassemia - mediterranean |
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HbS present how?
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mild to moderate sickle cell depending on amount of beta globin production
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how much beta globin chain does beta thalassemia major have?
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none!
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Lead poisoning leads to decrease in what and what change in cell appearance?
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decreased heme synthesis (decreased ferrochelatase and decreased ALA dehydratase)
basophilic stippling (because inhibits rRNA degredation) |
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increased iron, normal TIBC, increased ferratin?
tx? cell seen? |
sideroblastic anemia
B6 (pyridoxine) ringed sideroblasts (have iron-laden mitochondria) |
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sideroblastic anemia
1 hereditary cause and inheritance 2 reversible causes |
x-linked (aminolevulinic acid synthase deficiency)
reversible- lead, alcohol |
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lead poisoning changes seen (5 problems, 2 cell changes)
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LEAD
L- lead lines (Burton's lines) in gingiva, epiphyses of long bones E- encephalopathy A- sideroblastic anemia, abdominal colic D- drops (wrist and foot drop) sideroblasts, erythrocyte basophilic stippling |
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lead poisoning tx adults, kids
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adults- demercaprol, EDTA
kids- succimer (it sucks for kids to get lead poisoning) |
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megaloblastic anemia with increased homocysteine and increased methylmalonic acid
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B12 deficient anemia
(FOLIC ACID deficiency will have NORMAL METHYLMALONIC ACID) |
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hemolytic anemia, TMP-SMX cause what type of megaloblastic anemia
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folate-deficient
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Diphyllobacterium latum causes what type of anemia
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B12 megaloblastic anemia
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deficiency: peripheral neuropathy, loss of propioreception/vibration, dementia, spacticity,
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B12 deficiency
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metabolic disorders can cause what type of anemia?
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macrocytic anemias
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3 drugs that can cause macrocytic anemias
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5-FU, AZT, hydroxyurea
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in settings of paroxysmal notcturnal hemoglobinuria, aortic stenosis, prosthetic valves, normocytic, normochromatic anemias are result of what?
finding in urine? 2 findings in serum? |
intravascular hemolysis
hemoglobin in urine decreased haptoglobin, inc. LDH |
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jaundice in setting of hereditary spherocytosis, G6PD, sickle cell indicates what going on?
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extravascular hemolysis (RBCs being cleared by macrophages, increased unconjugated bilirubin building up)
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in Anemia of Chronic Disease, what substance increases? what cells decrease release of iron?
what are changes in levels of iron, TIBC, ferratin? |
hepcidin
macrophages dec. iron, dec. TIBC, inc. ferratin |
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if long standing disease, Anemia of Chronic Disease can go from normocytic, normochromatic anemia to
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microcytic, hypochromatic (like iron deficiency anemia)
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4 drug causes of aplastic anemia
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benzene, chloramphenicol, antimetabolites, alkylating agents (cyclophosphamide, nitrosoureas, Busulfan)
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4 viral causes of aplastic anemia
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parvo B19, HIV, HCV, EBV
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what inherited defect can cause aplastic anemia
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Fanconi's anemia (an inherited defect in DNA repair)
autosomal recessive, prevalent in Ashkenazi Jews |
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among other causes, aplastic anemia can be idiopathic or follow an acute bout of
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hepatitis
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aplastic anemia treatment growth factors used?
are immunosuppressive agents used in aplastic anemia treatment? |
G-CSF
GM-CSF yes (ex cyclosporine) |
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hereditary spherocytosis defects?
tx? |
ankrin, spectrin
splenectomy |
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back pain after ingestion of sulfa drug, infection, hemoglobinuria a few days later?
has decrease in what |
G6PD
glutathione |
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hemolytic anemia in a newborn is probably?
inheritance? |
Pryuvate kinase deficiency causes decrease ATP--> rigid RBCs --> extravascular hemolysis
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what is specific sickle cell mutation
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point mutation of glutamic acid to valine at position 6 on beta chain
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6 complications of sickle cell
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painful crisis (vaso-occlusive)
aplastic anemia (with parvo B19) salmonella osteomyelitis autosplenectomy splenic sequestration crisis renal medullary and papillary necrosis |
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2 renal complications in sickle cell
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renal papillary necrosis (from ischemia, most susceptible portion)
microhematuria (from medullary infarcts) |
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why does sickle cell not present at birth, and what is treatment for condition?
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because at birth, increased HbF and decreased HbS.
tx- hydroxyurea (increases HbF), bone marrow transplant |
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What is HbC defect, and how do HbSC patients present?
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HbC - glutamic acid--> Lysine mutation. HbSC patients have 1 of each, milder form of sickle cell.
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What is defect in Paroxysmal Nocturnal Hemoglobinuria, and how does it lead to hemolysis?
what lab value increased? intravascular or extravascular hemolysis? |
impaired GPI anchor synthesis (allows Decay Accelerating Factor which inhibits complement binding to dock on RBC membrane) so complement binds and lyses RBCs
increased hemosiderin lysed in blood vessels, so intravascular |
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3 causes warm agglutinin hemolytic anemia
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(IgG)
SLE CLL alpha-methyldopa |
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3 causes cold agglutinin hemolytic anemia
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(IgM)
CLL mycoplasma pneumoniae infectious mononucleosis |
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What is process of Direct Coomb's test?
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add anti IgG to serum to see if it binds to any IgG on RBC surface
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What is process of Indirect Coomb's test?
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add normal RBCs to patient serum, see if serum IgG agglutinates RBCs using anti-RBC surface Ig
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5 conditions microangiopathic anemia seen in
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- is hemolytic anemia due to narrowing/obstrcted lumen, produces schistocytes
TTP HUS DIC SLE malignant hyperthermia |
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2 causes of macroangiopathic extrinsic hemolytic anemia
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prosthetic valves, aortic stenosis
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2 infections that can cause hemolytic normocytic anemias
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malaria, babesia
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lab changes: iron deficiency
serum iron TIBC/transferrin Ferratin transferrin saturation (Fe/TIBC) |
serum iron - decreased (primary)
TIBC - increased Ferratin - decreased transferrin saturation - way down |
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lab changes: Anemia of Chronic Disease
serum iron TIBC/transferrin Ferratin transferrin % saturation |
serum iron - decrease
transferrin/TIBC- decrease ferratin - increase (primary) transferrin % saturation - normal |
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lab changes: hemachromatosis
serum iron TIBC/transferrin ferratin transferrin % saturation |
serum iron - increase (primary)
TIBC/Transferrin - decrease ferratin- increased transferrin % saturation - way up |
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lab changes: pregnancy/OCP use
serum iron transferrin/TIBC ferratin transferrin % saturation |
serum iron - normal
transferrin - increase (primary) ferratin- normal tranferrin % saturation - decrease |
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lab changes: lead poisoning
serum iron transferrin/TIBC ferratin transferrin % saturation (Fe/TIBC) |
serum iron - increased
transferrin/TIBC - decrease ferratin - normal (doesn't store lead) transferrin % saturation - increase |
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blistering cutaneous photosensitivity, tea colored-urine
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porphyria cutanea tarda
defect in uroporphyrinogen decarboxylase inhibits heme synthesis |
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protoporphyrin accumulation indicates what?
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lead poisoning
(inhibits ferrochetelase and ALA dehydratase) |
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build up of aminolevulinic acid (delta ALA) indicates what condition? tx?
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acute intermittent porphyria
(problem in heme synthesis, deficiency of porphyrobilinogen deaminase) tx- heme and glucose (inhibit ALA synthase) |
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in decreased heme synthesis, what enzyme is upregulated?
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ALA (aminolevulinic acid) synthase
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both porphyrias are problems in heme synthesis, and can cause buildup of uroporphyrin and dark urine. Which porphyria has neuropathy, and which has photosensitivity?
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acute intermittent porphyria (porphyrobiliongen deaminase) - polyneuropathy, pschy disturbances, and drug induction (urine is "red wine" colored)
porphyria cutanea tarda (uroporphyrinogen decarboxylase) - photosenstivity (urine is "tea colored") |
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vitamin K deficiency on PT, PTT
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increases both
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Hemophilia A and B:
defects? affect extrinsic or intrinsic pathway? |
A- factor VIII
B - factor IX intrinsic (only change PTT) |
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coagulation vs platelet disorders:
which get hemarthroses? bleeding gums? epistaxis? petechiae? purpura? |
hemarthroses - coagulation disorders
all others - platelet disorders |
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Bernard-Soulier disease is a bleeding disorder with what defect?
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defect in gpIb --> problem with platelet to collagen adhesion at site of injury
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what is the natural disorder analog to ticlopidine/clopidogrel?
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Glanzmann's thrombocytopenia (decrease in ADP-regulated gpIIb/IIIa expresion which causes decreased platelet-platelet aggregation)
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what is the disease analog to abciximab?
will see what cell finding? |
Idiopathic thrombocytopenic purpura
-idiopathic development of gpIIb/IIIa antibodies -increased megakarocytes |
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3 platelet disorders that have decreased platelet counts?
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-Idiopathic Thrombocytopenic Purpura (ab to gpIIb/IIIa)
-Thrombotic Thombocytopenic Purpura Bernard-Soulier Disease (gpIb deficiency) |
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neurologic symptoms
renal symptoms fever microangiopathic hemolysis thrombocytopenia? disease, deficiency |
Thombotic Thrombocytopenic Purpura
ADAMTS13 deficiency, leads to large multimers of vWF that increase platelet aggregation and thrombosis |
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von Willebrand's disease:
problem? inheritance? change in pT? pTT? BT? tx |
MOST COMMON BLEEDING DISORDER
decreased vWF leading to decreased collagen-platelet aggregation inheritance- autosomal dominant BT increased, pTT can be increased because vWF carries Factor VIII tx- desmopressin (releases endogenous vWF) |
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what will changes be in DIC?
BT platelet count PT PTT |
BT - increased
Platelet count- decreased PT- increased PTT- increased |
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DIC causes (7)
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STOP Making New Thrombi
Sepsis Trauma Obstetrical emergency acute Pancreatitis Malignancy Nephrotic syndome Transfusion |
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skin necrosis with hemorrhage seen after warfarin administration with what deficiency?
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Protein C or Protein S (decreased inactivity of V and VIII)
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what genetic deficiency causes decreased heparin effect?
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antithrombin III deficiency
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Prothrombin gene mutation is what and associated with higher inidences of what?
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3' untranslated region of prothrombin gene, leads to venous clots
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increased WBC count, left shift (ex. 80% bands), and increased leukocyte alkaline phosphatase due to infection is
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Leukemoid rxn, not leukemia
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Leukemia vs lymphoma:
which is usually discrete masses, which usually has cells found in peripheral blood |
Leukemia- lymphoid neoplasm with widespread involevment of bone marrow and peripheral cells
Lymphoma- discrete masses arising from lymphoid tissue |
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Hodgkins vs Non Hodgkins lymphoma:
spread/distribution symptoms epidemiology |
Hodgkins:
spread - single group of nodes, not extranodal involevement, contiguous spread symptoms - B symptoms prominent epidemiology - bimodal distribution (adolescent and older) Non-Hodgkin's lymphoma spread- multifocal with extranodal involvement symptoms- less B symptoms epidemiology- 20-40 years old |
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what is prognostic ratio for Hodgkin's lympoma?
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increased lymphocytes/decreased Reed Sternburg cells better prognosis
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Reed-Sternberg cell seen in?
50% of cases associated with what? |
Hodgkin's lymphoma
EBV infection |
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4 types of Hodgkin's lymphoma
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Nodular sclerosing (excellent prognosis)
Mixed Cellularity (intermediate prognosis) Lymphocyte Predominant (excellent prognosis) Lymphocyte depleted (poor prognosis) prognosis determined by ratio of lymphocyte to Reed Sternburg cells |
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Reed sternburg cell lymphoma with collagen banding and lacunar cells
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Nodular sclerosing type Hodgkins (most common, excellent prognosis, more common in women)
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lymphoma type with many lymphoctyes and reed sternburg cells
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mixed cellularity Hodgkin's Lymphoma (intermediate prognosis)
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lymphoma type with many lymphocytes and a few reed sternburg cells
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lymphocyte predominant Hodgkins (excellent prognosis, in younger men)
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lymphoma type with few lymphocytes, high lymphocyte/reed sternburg cell ratio
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lymphocyte depleted, poor prognosis (in older individuals)
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Burkitt's Lymphoma mutation and genes involved
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t(8:14)
c-myc moved to heavy chain Ig gene |
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Most common adult non-Hodgkin's lymphoma
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Diffuse large B-cell lymphoma
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lymphoma t(11:14), CD 5+
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Mantle Cell lymphoma (a non-Hodgkin's B-cell lymphoma)
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t(14:18) cancer and gene
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Follicular, bcl-2 antiapoptosis gene
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Adult T cell lymphoma caused by what virus
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HTLV-1 (present with cutaneous lesions, usually japanese, african, carribean)
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adult with cutaneous patches, diagnosed as mycosis fungoides is what
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a T cell non-hodgkin's lymphoma
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Multiple Myeloma
what seen in tissue? bone? urine? electrophoresis? blood? |
tissue- primary amyloidosis (AL)
bone- punched out lesions urine- Bence-Jones proteins (Ig light chains) electrophoresis- M spike (monoclonal) blood- rouleaux formation |
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CRAB used in for what condition
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Multiple myeloma
hyperCalcemia Renal Insufficiency Anemia Bone lytic lesions/Bence Jones Proteins |
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"fried egg" plasma cell appearance seen in
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Multiple Myeloma
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2 most common monoclonal Ig in Multiple myeloma
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IgG (50%), IgA (25%)
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2 conditions with M spike
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Waldenstroms macroglobinemia (increased IgM, viscosity symptoms, no bone lesions)
Multiple Myeloma |
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MGUS is M protein of less than ___ and plasma cells less than ____
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M protein less than 3 g/dL
10% of bone marrow |
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"Starry Sky"
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Burkitt's Lymphoma
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CD 30+ and CD 15+ cell
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Reed Sternberg cell (Hodgkin's lymphoma)
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early childhood leukemia
2 positive tumor cell markers 2 regions of spread |
ALL
markers - TdT+ and CALLA+ regions of spread- CNS, testes |
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t(12:21) is a positive prognostic indicator for what cancer
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ALL
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hairy projections on cells in elderly, stain Tartrate-Resistant Acid Phosphatase + is what cancer
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Hairy Cell Leukemia (TRAP+)
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person over 60 with smudge cells?
can get what type of anemia |
CLL/SLL
warm/cold antibody autoimmune hemolytic anemia |
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which leukemia has circulating myeloblasts on smear? treatment?
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AML
for AML M3 (PML), use vitamin A (all trans retinoic acid) because it induces differentiation of myeloblasts |
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increased neutrophils, metamyelocytes, basophils, splenomegaly, low leukocyte alkaline phosphatase?
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CML
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what are gene products of CML translocation?
drug mech for treatment? |
9:22 bcr-abl
bcr- serine/threonine kinase activity abl- tyrosine kinase treatment - imatinib bind abl's tyrosine kinase and inhibits its activity |
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approximate ages for Leukemia type onset:
<15 ~60 30-60 >60 |
<15 = AML
~ 60 = AML 30-60 = CML > 60 = CLL/SLL |
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name the leukemia based on predominant cell type:
lymphoblast myeloblast myeloid stem cell non-antibody producing B cell |
lymphoblast (pre T or pre B) - ALL
myeloblast - AML myeloid stem cell - CML (but can have blast crisis, and cells can tranform into lymphoblasts/myeloblasts--> ALL or AML) non-antibody producing B cells - CLL |
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treatment of AML M3 can cause release of auer rods, causing what
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DIC
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cells expressing s-100 and CD1a? have what granules
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Langerhans Cell Histiocytosis
(will have Birbeck granules, look like tennis rackets) |
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JAK 2 function, 3 disorders associated with its mutation
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tyrosine kinase involved in hemapoetic stem cell signaling
Polycythemia Vera Essential Thrombocytosis Myelofibrosis |
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What is increased in polycythemia vera, and mutation associated
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RBCs, WBCs, platetets
JAK2 mutation |
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3 conditions resulting in absolute polycythemia
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high altitude, lung disease, congenital heart disease
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5 conditions that result in polycythemia vera
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Renal cell carcinoma
Hepatocellular Carcinoma Wilm's tumor cyst hydronephrosis |
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lab changes: polycythemia vera
plasma volume RBC mass O2 saturation Epo |
plasma volume - increase
RBC mass - way high 02 saturation - normal Epo - decrease |
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lab changes: appropriate absolute polycythemia
plasma volume RBC mass 02 saturation Epo |
plasma volume - normal
RBC mass - increase )2 saturation - decrease (primary) Epo - increase |
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lab changes: inappropriate absolute polycythemia
plasma volume RBC mass O2 saturation Epo |
plasma volume - normal
RBC mass - increase O2 saturation - normal Epo - increase (ectopic) |
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lab changes: relative polycythemia vera
plasma volume RBC mass O2 saturation Epo |
Plasma volume - decrease
RBC mass - normal O2 saturation - normal Epo - normal |
