ch21: alterations of hematologic function Flashcards
anemia
low on RBCs, antimitotic chemo
- decrease in # of circulating RBCs
- decrease in quality/quantity of Hgb
what is the main result of anemia
tissue hypoxia
hypoxemia
O2 deprivation in the blood
- altered production of RBCs
- blood loss
- increased destruction of RBCs
-cytic
alteration in cell size
normocytic
blood cells all normally sized, just might not have enough
macrocytic
blood cells largely sized
microcytic
blood cells small in size
-chromic
alteration in Hgb concentration
normochromic
normal amount of Hgb
hypochromic
Hgb amounts are too little
hyperchromic
Hgb amounts are too much
anisocytosis
all RBCs are diff shapes
poikilocytosis
all red blood cells are diff shapes
macrocytic-normochromic anemias
large cells, but normal Hgb amount
- pernicious anemia
- folate deficiency anemia
pernicious anemia
deficiency of absorption of vitamin b12
what is the purpose of vitamin b12
needed for RBC production
what is intrinsic factor and where is it made?
made in stomach to help absorption of b12
folate deficiency anemia
decreased folic acid
what is the purpose of folic acid
for DNA synthesis
t/f: b and c vitamin are water soluble which means you can excrete them through urine
true
microcytic-hypochromic anemias
small cells, too little Hgb amounts
- iron deficiency anemia
- sideroblastic anemia
- thalassemias
iron deficiency anemia
- signs
- treatment
too little iron
signs: corners of mouth broken, dark circles around eyes
treatment: iron supplements
sideroblastic anemia
metabolic disorder; ineffective utilization of iron during erythropoiesis –> iron accumulation
“iron stuffed mitochondria”
thalassemias
similar to sickle cell anemia; both are mutations in hemoglobin that lead to malformed hemoglobin (but thalassemia does NOT malformed cell)
what is the most common type of thalassemia
beta thalassemia: mutation in beta subunits of hemoglobin that leads to small hgb and iron deficiency
what is the difference between sickle cell anemia and thalassemia?
thalassemia: mutated hgb but not malformed cell
sickle cell: mutated hgb with malformed cell
normocytic-normochromic anemias
normal cell size, normal Hgb number
- aplastic anemia
- hemolytic anemia
- hemolytic disease of the newborn (HDN)
- posthemorrhagic anemia
- anemia of chronic inflammation
- sickle cell anemia
aplastic anemia
- treat?
cells might look normal but don’t have enough due to problem at bone marrow
- treat by diet (palliative measures)
hemolytic anemia
- hereditary vs acquired
something is causing lysis of RBCs
- heredity: due to genetics
- acquired: infectious disease
hemolytic disease of the newborn (HDN)
- what should the mom get injected with to prevent this?
Rh negative mom has antibodies that can attack Rh positive baby
- mother needs to be injected with RHOGAM
what is RHOGAM
shot of Rh factor - sticks to Rh positive antibodies so they don’t cross the placenta
posthemmorhagic anemia
lost a lot of blood = low on RBCs
anemia of chronic inflammation
cytokines down regulate processes that synthesizes all bone marrow cells
sickle cell anemia
RBCs abnormally shaped due to a mutated hemoglobin protein
- resistance to malaria
myeloproliferative RBC disorders
- polycythemia
- polycythemia vera
- iron overload
polycythemia
too many RBCs –> many problems and dysfunctions
relative polycythemia
appear to have a high [ ] of RBCs when you really don’t (dehydration)
absolute polycythemia
where number of RBCs are truly elevated
primary absolute polycythemia
problem in bone marrow leads to too many RBCs (polycythemia vera)
secondary absolute polycythemia
Hyperactivity with Erythropoietin (EPO) → hormone produced that triggers RBC production; made by kidney
where is erythropoietin produced
in the kidney
polycythemia vera
increased # of RBCs due to a bone marrow problem –> results to thick and sticky blood
clinical manifestations of polycythemia vera?
- ischemia/infarction of tissue
- petechial rash
- JAK2 mutation
iron overload
too much iron in diet, but can also be a disease condition
hereditary hemochromatosis
too much iron (can’t process iron properly) but through GENETICS and not DIET
t/f: blood drawn for pt with hereditary hemochromatosis can still be used
false
leukopenia
WBC deficiency (granulocytopenia [eosinopenia, basophenia], pancytopenia, lymphocytopenia)
leukocytosis
overabundance of WBCs
granulocytosis, eosinophilia, basophilia
what is the leukemoid reaction
“shift to the left” during leukocytosis; RESEMBLES leukemia but NOT due to a malignant condition of the bone marrow
can just be a response to infectious disease
when do you see eosinophilia
parasitic infections
yes/no: can you see tumors during dysfunctions of the blood?
no
leukemia
producing too many blood cells; MALIGNANT disorder of blood and bone marrow
what is the hallmark sign of leukemia
increased WBC proliferation (that aren’t made right)
leukemia usually results in _______ (describe it)
pancytopenia: corresponding decrease in other cells (too much WBC, not much RBC or platelets)
acute lymphocytic leukemia (ALL)
rapidly developing abnormally high number of malformed lymphocytes
acute myelogenous leukemia (AML)
rapidly developing abnormally high overabundance of cells of myeloid lineage
chronic lymphocytic leukemia (CLL)
gradual developing abnormally high number of malformed lymphocytes
chroni myelogenous leukemia (CML)
gradual developing abnormally high overabundance of cells of myeloid lineage
what happens to chromosomes during CML?
philadelphia translocation: eciprocal translocation over across a couple of chromosomes (almost always seen in ppl with CML)
-Segments of chromosome 9 and 22 switching places with each other
Not good for cells (don’t want crossovers between diff)
lymphadenopathy
dysfunction of the lymphatic system
