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what is hemophilia
bleed too damn much
what is hematocrit
% of rbc’s
what is plasma made of
water, proteins, nutrients, hormones, waste, na, cl, k
what is anemia
too little hematocrit
what is polycythemia
hematocrit too high, blood may be too thick
what do rbc’s come from
reticulocytes
what do platelets come from
megakaryocytes
how do you make tissue macrophage
blast cells → monocytes → tissue macrophage
how do you make neutrophils
blast cells → promyelocyte → band cell → neutrophil
what do B and T lymphocytes come from
bone marrow lymphocyte precursors
*how long do rbcs stay in circulation
120 days
*what is A1C and why is it measured in diabetic patients every 3-4 months
its the amount of sugar carried on 1 hemoglobin, which lives for 120 days. allows providers to see a “average blood sugar” instead of just the patients current blood sugar
*what does MCV measure
how big each rbc is
*what does low MCV mean
anemia caused by chronic kidney disease
*what does MHC measure
average amount of hemoglobin in rbcs
*what does low mhc mean
hypochromic anemia
*what does high mhc mean
dehydration, hemolytic anemia
what is a retic count measuring
% of immature rbcs in blood
what does a high retic count mean
bone marrow is making more rbc’s and trying to fix anemia
what makes up rbcs
2 alpha chains, 2 beta chains, 4 heme groups that hold iron
*what are high neutrophil levels associated with
BACTERIAL INFECTIONS
*what are high lymphocyte levels associated w
viral infections
*what are high monocyte levels associated with
fungal infections, TB
*what are high eosinophil levels associated with
allergic reactions, autoimmune disorders, parasites
*what are high basophils levels associated with
cancer
*what is low platelet count associated with
chronic liver disease
*what is dec production of rbcs associated with
bone marrow failure (APLASTIC ANEMIA)
what nutrient deficiencies may lead to anemia
iron, B12, folate, protein
what do low levels of B12 or folate mean
megaloblastic anemia
what is the most common nutrient deficiency in the world
iron (microblastic hypochronic)
what does protein deficient anemia entail
decreased formation of all homopoetic cells, liver cirrhosis bc liver cant make proteins and thus all cells are protein deficient
what are examples of genetic hemoglobinopathies that lead to weird hemoglobin and rbc shapes
sickle cell anemia, thalassemia
what is an example of structural preotein defects that lead to abnormal rbc shapes
spherocytosis
causes of increased loss or death of rbcs
bleeding, immune hemolytic anemia, hypersplenism, malaria
microcytic hypochronic anemia =
iron deficient anemia
macrocytic normochromic anemia=
b12 deficient (vegans, gastric bypasses)
*what does dec wbc and platelets mean, how is it treated
pancytopenia, need transplanted stem cells
causes of aplastic anemia
idiopathy (most common) or secondary bc of chemo, radiation or a viral infection
clinical features and treatment for aplastic anemia
recurrent infections bc of pancytopenia and bleeding, need a bone marrow transplant
clinical features and treatment for iron deficient anemia
pale, tired, dyspnea. stop the bleeding and get em some iron
causes of iron deficient anemia
inc loss of iron, dec intake or absorption of iron, inc iron needs
what would inc loss or iron
chronic bleeding, menorrhagia, bleeding ulcer, use too many NSAIDS, hookworms
what would cause dec iron intake/absorption
malnutrition (intake), chrons, celiac, inc use of antiacids
what would cause inc iron requirement
being preg, growing kids/teens, period
where is 60-80% of bodys iron
in rbcs
what is iron doing as its metabolized
most bound to ferratin or transferatin going to live/bone marrow
what binds to b12 after its separated from protein by acid during its metabolism
intrinsic factor
*causes of megaloblastic anemia
pernicious- atrophic gastritis and lack of intrinsic factor antibodies prevent binding of b12 to the intrinsic factor, gastric bypass, celiac, chrons
what do pernicious megaloblasic anemai look llike in bone marrow
bone marrow is hypercellular and has lots of megaloblasts, decreased but huge rbcs
what happens if you dont treat pernicious megaloblastic anemia
spinal cord disease, demyelination and neuro symptoms if severe
clinical features and treatment of megaloblastic anemia
tired, pale, sob, weak, hard to walk and look watch their own legs when they walk. loss of proprioception, deep tendon reflexes and sense of vibration. spinal cord issues if severe. need folate or b12 supplements
causes of hemolytic anemias
structural abnormalities or infection, leading to rbc destruction
common features of hemolytic anemias
reduced rbc lifespan, inc erythropoietin, erythroid hyperplasia*, byperbilirubenemia, jaundice
what causes sickle cell anemia
genetic, an abnormal hemoglobin S gene in some or all rbcs
% of rbcs w hemoglobin S mutation and associated symptoms
less than 40%- asymptomatic
40-80%- mild symptoms
80%+- severe symptoms
what can lead to sickling crisis’s (flare ups of sickle cell anemia)
sickness, low o2 pressure, hard workouts, pregnancy
clinical features of sickle cell anemia
dec/slow intellectual development and neurologic deficits, cardiopulmonary insuffciency, recurrent infections, anemia, elevated bilirubin
*cause of thalassemia
genetic defect in synthesis of HbA so less globin is made
which kind of thalassemia is worst (and more common) and why
T beta, bc only two beta chains so harder to compensate if one is fucked, but you have 4 alpha chains so if one or two are fucked its easier to compensate
clinical features of thalassemia
microcytic, hypochromic. slow growth, T major specifically- hepatosplenomegaly hemosiderosis (iron overload)
treatment for thalassemia
no cure, T minor- no treatment needed, T major- kids will die from lack of hemoglobin unless transfused
causes of hereditary spherocytosis
genetic defect of structural proteins of rbcs, causes membrane destabilization and lysis in spleen, big ass round spherocytes cant get into tiny capillaries
clinical features of hereditary spherocytosis
typical anemia shit, splenomegaly and jaundice from the hemolysis
treatment for hereditary spherocytosis
splenectomy (doesnt fix the spherocytes not being able to go into capillaries tho)
causes of immune hemolytic anemia
IgG binds to rbc autoantigen/neoantigen→ activates compliment→ rbc lysis
clinical features of immune hemolytic anemia
splenomegaly, jaundice, rapid drop of Hb
*causes of polycythemia
neoplastic (cancer of blood, most common), blood doping
clinical features of polycythemia
hyperviscosity, clots easy, hypertension bc too much blood in vessels, flushed, erythroid hyperplasia in bone marrow, bone marrow cells look weird
treatment for polycythemia
phlebotomy, chemo drugs
*neutrophils are _%
54-62%
*lymphocytes are _%
25-33%
*monocytes are _%
3-9%
*eosinophils are _%
1-3%
*basophils are _%
less than 1%
*hemolytic anemia intracorpuscular defects cause
structural abnormalities
*hemolytic anemia extracorpuscular defects cause
antibodies (transfusion rxn or autoantibodies), infection, mechanical factors
*causes of leukopenia
can be part of aplastic anemia (presents as pancytopenia), chemo, environment, radiation
clinical features of leukopenia
neutropenia → frequent bacterial infections
lymphopenia → frequent bacterial, viral, fungal and/or parasitic infections bc low lymphocyte amount
long term may be fatal
leukopenia treatment
stop exposure to whatever is causing it or give poietins to inc rbc prod
what does persistent leukocytosis look like and need
giant tender lymph node in neck of kid/teen that doesnt respond to antibiotics, may need a biopsy
wbc and plasma malignancies causes
idiopathic or caused by a virus
wbc and plasma malignancies clinical features
bone marrow infiltration by malignant cells, inc number of immature blood cells, anemia, recurrent infections, uncontrolled bleeding, neoplastic stem cells show genetic changes
*acute lymphocytic leukemia epidemiology
20% of all leukemias but most common leukemia in kids, rapid progression, peaks age 5, bad prognosis in elderly
*acute myoloid leukemia epidemiology
*auer rods on smear, most common acute leukemia in adults mostly elderly, 40% of all leukemias, myeloproliferative disease, w/o treatment 6mo survival, w treatment 15-30%
acute myoloid leukemia classification
AML w recurrent genetic abnormalities, AML evolving from multilineage dysplasia, AML not otherwise specified
acute myoloid leukemia treatment
chemo, high dose irradiation, bone marrow transplant
chronic myoloid leukemia epidemiology
15% of all leukemias, rare before adolescence, incidence inc w age , most pts die in 3 yrs, malignant disease of pluripotent hematopoietic stem cells (90% philadelphia better prognosis)(most promising is gleevec- 90%)
chronic myoloid leukemia clinical features
slow onset, mild anemia, hypermetabolism, tire easily, prone to infections, splenomegaly and clotting
chronic phase of chronic myoloid leukemia
2-3yrs, marked leukocytosis, bone marrow < 10 blasts, inc platelets in bone marrow
accelerated phase of chronic myoloid leukemia
(1/2 pts) over 10% blasts in bone marrow, over 20% basophils in blood, increasingly unresponsive to treatment, ends in blast crisis
sudden onset blast crisis phase of chronic myoloid leukemia
other (1/2 pts), cant be treated, dead
chronic lymphocytic leukemia epidemiology
25% of all leukemias, most over 50, slow progression, can transform into another leukemia with less favorable prognosis
chronic lymphocytic leukemia clinical features
smudge cells on smear, indistinguishable from normal lymphs, similar to small-cell lymphocytic lymphoma
chronic lymphocytic leukemia treatment
unresponsive to chemo
*lymphomas epidemiology
3% of all malignant disease, no benign ones, most lymphomas have a B-cell phenotype, all ages, often infiltrate the lymph nodes/spleen/thymus/bone marrow, diagnosed by lymph node biopsy w light microscopy
non hodgkins lymphoma most often involves what
lymph nodes, bone marrow, spleen, and thymus but can be extranodal (GI)
clinical features of non hodkins lymphoma
lymph node enlargement (solo or diffuse), tired, fever, weight loss, sweating, anemia, leukopenia, infections
features of follicular non hodgkins lymphoma
most common in US, most common in elderly, slow growing, usually mild constitutional, chemo ineffective, in terminal stage body overwhelmed by tumor burden
features of diffuse large B cells non hodgkins lymphoma
several forms, most common aggressive NHL, tumor cells spread, chemo works
features of burkitts non hodgkins lymphoma
highly malignant, cells prone to apoptosis, chemo works, most can be totally cured, common in sub saharan africa bc epstein bar virus epidemic, kids and young adults