hematoligic disorders Flashcards
hgb
14-18g/100ml
12-16g/100ml
HCT measures the % of a given volume of whole blood, that is occupied by erothrocytes
40-54%
37-47%
TIBC
250-450ug/dl
serum Iron
50 to 150ug/dl
MCV- average size of the indivual erythrocyte
80-100fl
MCH average amount and weight of HGB in a single erythrocyte
26-34pg
microcytic
less than 80 MCV
normocytic
80 to 100 MCV
macrocytic
over 100 mcv
Mean corpuscular HGB concentration MCHC
32-36% expression of average hgb concentratio or proportion of each RBC occupied by HGB as a percentage more accurate than MCH
hypochromic MCHC
less than 32%
normochromic MCHC
32 - 36%
hyperchromic MCHC
over 36 contraversial
Low MCV less than 80
iron defficiency anemia and thalassemia
high MCV anemia greater than 100
b12 or folate defficiency, etoh, liver failure and drugs
normocytic MCV 80-100 anemia
anemia of charonic disease, sickle cell, renal faiure, blood loss, hemolysis
iron defficiency anemia
low MCV less than 80
most common cause
decreased IRON for RBC formation
caused by blood loss, inadequate iron intake or impaired absorption.
Iron defficiency anemia S and S
few sx with HCT over 30 pica dypsnea with mild exercise HA postural hypotensioin pallor palpitations tacchy
IRON deff anemia Labs
MCV less than 80
low MCHC less than 32
“micro hypo”
High TIBC- 240 to 450 micrograms per deciliter (mcg/dL).
serum ferritin is low 12 to 300 nanograms per milliliter of blood (ng/mL) for males and 12 to 150 ng/mL for females.
iron defff not most common anemia in one pop
gero (anemia of chronic disease)
Iron defficiency anemia tx
oral ferrous sulfate- 300-325 1-2hrs after meals
dont take with antacids
take with vitamin C
rasins, geen vegies, red meats, citrus products,
Thalassemia def
genetically inherited disorders resulting in abnormal HGB production resulting in microcytic MCV less than 80 hypochromic MCHC less than 32.
mediterianina african, indian etc
normal TIBC 240 to 450 micrograms per deciliter (mcg/dL).
Normal serum ferritin 12 to 300 nanograms per milliliter of blood (ng/mL) for males and 12 to 150 ng/mL for females.
thalassemia treatment
not much, dont give iron, RBC way later on
splenectomy way way down the road
Folic acid deficiency def
macrocytic MCV over 100, normochromic 32-36 due to folic acid deficiency or mal absorption
Folic acid deficiency anemia s and s
NO NEUROLOGICAL SIGNS ARE SEEN WHICH IS DIFFERENT FROM B12
glossitis
fatigue,
low folate levels Adults - 2-20 ng/mL, 2-20 μg/L, or 4.5-45.3 nmol/L.
he lists red blood cell folate less than 100ng/ml
HCT and RBC decreased
folic acid deficiency anemia treatment
folate 1mg orally daily
bananans, peanut butter, fish green leafy veggies, iron fortified breads and cereal
pernicious anemia def
macrocytic MCV over 100, normochromic MCHC 32-36 anemia due to deficiency of intrinsic factory which results in mal absorption of B12
pernicious anemia def
glossitis- big beefy red tongue lss of vibratory sense loss of fine motor control positive romberg positive babinski dizzy annorexhea
pernicious anemai labs
low hgb, hct, adn RBC's MCV is increased over 100 serum b12 is less that 01 mcg/ml anti-IF and antipareietal cell atntibody test affirms a deficiency schilling test may help determine cause
pernicious anemia treatment
B12 100mch im daily for one week
lifelong monthly admin may be indicated
anemia of chronic disease
chronic MCV 80-100 MCHC 32-36 associated with chronic inflammation, infection, renal failure or malignancy - associated with decreased erythrocyte life span.
SECOND MOST LIKELY CAUSE OF ANEMIA
SERUM IRON AND TIBC LOW serum Ferritin is high serum ferritin 12 to 300 nanograms per milliliter of blood (ng/mL) for males and 12 to 150 ng/mL for females.
and TIBC is low normal TIBC 240 to 450 micrograms per deciliter (mcg/dL).
sickle cell anemia
chronic hemolytic anemia that is genetically transmitted by sickle shaped RBC
an acute periodic exacerbation in which RBC’s become sickle shaped and cause obstruction
cellular hypoxia, results in acidosis and tissue iscemia
pain occurs from tissure ischemia, and blood hyperviscoisty
factors that percipitate sickling
hypoxia, infections, high altitudes, dehydration, physical or emotional stress, surgery, blood loss, acidosis.
sickle cell s and s
increased succeptability to infection
sudden onset pain in chest back and abdomen
joint pain
sickle cell labs
HGB down, preipehral smear shows sickle shaped RBC’s
celulose acetate and cirate agar gel electrophoresis to confirm HGN genotype
sickle cell treatment
acute - fluids for dehydration
analgesics for pain, o2 for hypoxemia
von villebrand disease
reduced ability to produce blood clots (genetic) deficiency in clotting factory VIII 8
S and S
frequent prolonged or sever episodes of bleeding
easy brusing
management isdesmopressin, adding factor 8
leukemia
neoplasms arising from hematopoietic cells in bone marrow
leukemia
more frequent in males,
leukemia ANL/AML
acute nonlymphocytic anemia/ acute myelogenous leukemia
80% of leukemia in adults
remission from 50% to 80%
long term survival is 40%
leukemia ALL
acute lymphocytic lukemia
more difficult to treat in adults than in kids
HALLMARK OF DISEASE IS PANCYTOPENIA WITH CIRCULATING BLASTS
leukemia CLL
chronic lymphocytic leukemia most common leuk in adults occurs in middle and old age median survival is 10 years LYMPHOCYTOSIS IS HALLMARK OF THE DISEASE
Chronic myelogenous leukemia
CML
most often 40 or older
median survival is 3-4 years
HALLMARK IS PHILADELPHIA CHROMOSOME seen in leukemic cells
leukemia s and s
may be asymptomatic
cancer stuff
generalzed lymphadenopathy
leukemia labs
CBC with subnormal RBCs and neurtrophils
elevated ESR
peripheral blood smear differentiates between acute and chronic
NEED BONE MARROW ASPIRATION TO CONFIRM DIAGNOSIS
leukemia management
chemo- use allopurinot to reduce tumor lysis syndorme in high risk patients
bone marro transplant
control of symptoms
Lymphoas
lymphocytic malignancy
diagnoses by biopsy of enlarged lymph nodes
lymphoma stage 1-4
lymphoma stage 1: localized to single node or group
2 more than one node or group, confined to one side of diaphragm
3nodes or spleen involved, both sides of the diaphragm
4. liver or bone marrow involvmentt.
when to generally biopsy a node
any node greater than one cm, not associated with infection lasting more than 4-6weeks
non hodgkins lymphoma
may be viral cause, unknown presents with lymphadenopathy most common neoplasm between 20-40 years of age less predictable patten of spread advanced stage is usually apparent
hodgkins disease
cause is unknown
more commmon in males around 32 years of age
usually presents iwth cervical adenopathy and spreads in a predictable fashion along lymphy node groups\
CHARACTERISTIC REED STERNBERG CELLS DIFFERENTIATE FROM NON HODGKINS DISEASE
HODG AND NON HODGE DX
ct, xray, mri used to locate and stage
BIOPSY AND HISTOPATHOLOGIC EXAM USEED TO CONFIRM DX
hodg and non hodge treatment
radiation, chemo, bone marro transplant.
ITP
thrombocytopenia resulting from autoimmune destruction of platelets with or without supression of thrombopoiesis
ITP concepts
usually chronic, only occasionally requiring hospitilaization, women outumber men 3-1
ITP labs and diagnostics
bone marro analysis
low platelet count 150,000 to 450,000 platelets
with other causes of thrombocytopenia ruled out,
ITP management
may not need to treat untill plt is less than 20K
high dose steroids can push up count in a few days
iv gamma globulin, works quickly as well
gamm glob is preferred inHIV patients
patlet transfuison may help as well
ITP thrombocytopenic precautions
avoid constipaiton
no floos or shaving
hold pressure for 5 mins on cuts or line insertion
HIT
argatroban, lipirudin (refuldan
how to differentiate ITP from SLE as both have thrombocytopenia
bone marrow aspiration will tell u
DIC - acuired coagulation defficiency intravascular activation of coag and fibrinolytic systems thrombin and plasmin are activated, causing
simultaneous thrombus and hemorrhage- mortality is 50-85%
DIC is associated with
malignant neoplasm burns shock obestrical complicaitons acute leukemia liver disease
DIC pathophys
thrombin causes conversion of fibrinogen to fibrin, producing fibrin clots and microcoagulation
coagulation factors IE fibrinogen, prothrombin, platelets, factor 5, and 8 are thus reduced
criculating plasmin, activates the firinolytic system which lyses fibrin clots tion fibrin degradation products
hemmorhage results from the anticoagulant activity of Fibrin degradation products and the depletion of coagulation factors
DIC s and S
DIC variens greatly in severity
petechiae and mucous membrane bleeding
DIC labs
thrombocytopenia Plat less than 150k
decreased RBCs
hypo fibrinogen less thant 170mg/dl
increased fibrin degradation products over 45mcg/ml or rpresent at over 1:100 dilution
pt over 19 seconds
ptt over 42 second
d dimer positive at 1:8 dilution reflects simultaneous activation of thrombin and plasmin
increased FDP’s gives a predictive accuracy of 96% for diagnosing DIC
DIC treatment
treat the underlying condition and control the bleeding
platelet transfusions for thrombocytopenia
FFP for clotting factors
cryoparticiate to maintain fibrinogen levels are givenif bleeding is severe
use of heparin remains contriversial
therapy is aimed at cessation of bleeding and increasing plasma fibrinogen, and platelet count and decreasng FDP’s
