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122 Cards in this Set

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Classify the following:
1. Chronic lead poisoning
2. Chemotherapy (folate antagonist)
3. Myxedema
4. Bone marrow failure
5. Folate deficiency
6. Sideroblastic anemia
7. Chronic Renal disease
1. Hypo micro
2. Macro
3. N & N
4. N & N
5. Macro
6. Hypo Micro
7. N & N
Classify the following (2):
1. B12 deficiency
2. Thalassemias
3. Chronic disease
4. Iron deficiency
5. Chronic liver disease
(2)
1. Macro
2. Hypo Micro
3. Hypo Micro & N & N
4. Hypo Micro
5. N & N
What does the body need to absorb iron?
vitamin C & gastric acid
What are the most common causes of IDA?
chronic blood loss, diet, impaired absorption, & increased demand
Restless leg syndrome at night & pica are signs of __
Iron deficiency anemia
In IDA, what happens to:
Serum Fe
Ferritin
Bone marrow stores
TIBC
RDW
Serum Fe is DEC
Ferritin is DEC
Bone marrow stores DEPLETED
TIBC is INC
RDW is INC
What signs & symptoms are seen in IDA
Mostly asymptomatic!
fatigue, glossitis (slick), spooning of nails, Plummer-Vinson syndrome, chylosis
Tx for IDA
Ferrous sulfate, ascorbic acid, iron dextran
When should you see a retic response & Hgb response in IDA after tx
retic in 10-14 days (if anemia is recent)
Hgb in 2-3 weeks
Unable to recirculate iron in which anemia
Chronic disease
What are the primary diseases that chronic disease anemia is associated with
chronic inflammation, malignancy, connective tissue disorder, acute infections
In chronic disease anemia:
typical Hgb
Fe
Ferritin
TIBC
mild anemia (>10Gms)
Fe DEC
Ferritin INC
TIBC DEC
What is treatment for Chronic disease anemia
may give trial of Fe

TREAT UNDERLYING DISEASE
Pathophysiology-
ineffective erythropoesis secondary to abnormal pyridoxine metabolism
sideroblastic anemia
etiology of sideroblastic
idiopathic, hereditary, acute alcohol, isonyazide
Dx of Sideroblastic:
Serum Fe
Ferritin
TIBC
Serum Fe INC
Ferritin INC
TIBC DEC
See ringed sideroblasts in bone marrow in
sideroblastic anemia
see dimorphism in
sideroblastic anemia
Tx for sideroblastic
pyridoxine
pathophysiology-
beta chain of Hgb; defective erythropoesis, increased destruction
thalassemia
etiology of thalassemia
hereditary:
heterozygous-mild
homozygous-severe
Seen mainly in Meditteranean people
Thalassemia
See what in mild thalassemia
innocuous, micro hypo only
See what in severe thalassemia
spleenomegaly, hepatomegaly, abn development w/ growth retardation, endocrinopathies, etc.
When do you die w/ severe thalassemia
1st or 2nd decade of life
In severe thalassemia, it frequently combines w/ what type Hgb
S or C
What is tx for severe thalassemia
transfusion, chelating agents, BM transplant in children
Thalassemia:
Fe
Ferritin
TIBC
RDW
FE NORM
Ferritin INC
TIBC NORM
RDW NORM
__ & __ are necessary for DNA synthesis
Folate & B12
This deficiency cas cause depression & cognitive defects
Folate
This deficiency can cause demyelination of posterior column of spinal cord (vibratory sensation & sense of position), may be ataxic`
B12
what must you have to absorb B12
low gastric pH & intrinsic factor
etiology of B12 deficiency
absent intrinsic factor
dietary-rare, body has 3 year store
malabsorption (tropical/nontropical spure, pernicious anemia, fish, tape worm, parasites, malignancies, chemotherapy, etc.)
etiology of folate deficiency
dietary-most common, only 3 mo reserve
increased demand-pregnancy
malabsorption
Other causes of megaloblastic anemia
hemopoietic malignancies, drugs that interfere w/ DNA synthesis (5-fluorouracil, unknown etiology)
this is caused by lack of intrinsic factor
pernicious anemia
Signs & Symptoms:
+ Labinsky sign, sore tongue (beefy), numbness, & tingling in extremities
pernicious anemia
Signs & symptoms:
lemon colored pallor, nausea, diarrhea, anorexia, neurologic-post column (VS & SOP), tend to get vitiligo, depression, onset in 6th decade of life
pernicious anemia
In the lab, see
MCV > 95 & hypersegmented polys (>4)
pernicious anemia
In pernicious anemia, what does bone marrow look like
megaloblastic
How do you dx Pernicious anemia
1. Trial of B12 (give shot, come back in wk & look at retic count)
2. Schilling test
3. MMA & Homocysteine
4. Intrinsic factor antibodies & parietal cell antibodies
How does Schilling test work
1cc of B12 IM to saturate binding site
1. labeled B12 by mouth-check urine
if there-not pernicious
not there-Stage 2 (not absorbed)
2. labeled B12 & intrinsic factor
if there-pernicious anemia
not there-malabsorption, may be infection, give antibiotic for 10 days & repeat test; if still not there then in ileum , refer
How does Methylmalonic Acid (MMA) & Homocysteine work
both are increased in pernicious anemia; in folate def. MMA is norm & Homo is increased
How does intrinsic factor antibodies & parietal cell antibodies work
if both are positive, then 85% sure that it's pernicious anemia
Tx of pernicious anemia
B12 (1mg wk for 6 wks, then 1 mg month for life); if b/c of malabsorption, do injection of B12

Folate def. (1 tablet every day
disorder of the stem cell in which insufficient # of blood cells are produced (life threatening)
aplastic anemia
What do you see pancytopenia in
aplastic anemia
in aplastic anemia, what blood cells are deficient
erythrocytes, leukocytes, & thrombocytes
What is retic count like in aplastic
low
There is a dry tap if trying to get bone marrow in what anemia
aplastic
etiology of aplastic anemia
drugs: not dose related (dilantin, chloromycetin)

chemicals: benzene containing

viral: hep C, HIV, Eps Barr

immunologic: Lupus, myast gravis

congenital: phanconas anemia

BM replacement: w/ cancer cell, mylobibrosis, sarcoid
What 3 emias/penias do you see in aplastic
anemia, neutropenia, thrombocytopenia
Tx of mild aplastic
remove offending agent, support, steroids, packed RBC, platelet transfusion
Tx of severe aplastic
BM transplant (before transfusion), drugs (androgen, steriod, immunosup, antithymotic)
In the lab, you see spherocytes, poikilocytes, & heinz bodies in what
G6PD hemolytic anemia
In G6PD, what does
Retic
LDH
G6PD
look like
Retic INC
LDH INC
G6PD (during hemolysis, will be norm, low in mature cells, if high, not accurate)
Etiology of G6PD
exposure-to certain drugs(sulfas, mothballs, negram, furodantin), severe hepatitis, diab ketoacidosis, oxidative stress
Definition: abnormal hgb caused by recessive autosomal gene
Sickle cell anemia
Hgb AS =
sicle cell trait
Hgb SS =
Sickle cell disease
In sickel cell dz, pale, yellow mm, gall stones, systolic murmur, cardiomegaly, & CHF are due to
hemolysis
In sickle cell dz, hepatomegaly, chest syndrome (looks like pneumonia) is due to
vaso-occlusion
What is tx of sickle cell anemia
nutrition, immunizations (flu shot & pneumonia shot), folate daily, reduced exertion
Tx for sickle cell crisis
hydration, pain relief, exchange transfusion, hydroxyurea?(inc hgb F)
Herediatry membrane defect that increases osmotic fragility
spherocytosis (also elliptocytosis)
What might you see w/ spherocytosis clinically
mild anemia to severe hemolysis
gall stones
chronic leg ulcers
(won't see a lot of this)
Spherocytosis Lab:
Retic
LDH
Bili
MCV
MCHC
Inc retic
Inc LDH
Inc Bili
low MCV
Inc MCHC
Sphereocytes present
Tx of spherocytosis
spleenectomy, cholecystectomy, immunizations
Fragmentation w/ abn microcirculation, abn cardiac valves, A-V fistulas
microangiopathic hemolytic anemia
etiology of microangiopathic hemolytic anemia
DIC, prosthetic valves, March hemoglobinuria
Lab for microangiopathic hemolytic anemia

& tx
anemia & inc retic

tx underlying cause
Have positive Coombs in what 2 diseases
Warm antibodies & cold agglutinins
What is main thing wrong in warm antibodies autoimmune hemolytic anemia
spleenomegaly
Tx for warm antibodies
steroids to spleenectomy to immunosup drugs
lymphoproliferative disease
cold agglutinins
mycoplasma pneu & SLE associated w/ what anemia
cold agglutinin
tx for cold agglutinin
none
drug induced immune hemolytic anemia can be caused by
weeks to months of aldomet
85% of adult leukemias
AML
Classification of AML
FAB M1-M7
M2 w/ t(8;21)-maturation, good px
M3-promyelocytic (except for acute promyelocytic); good px
M5, M6, M7-poor px
most important prognostic feature of AML
cytogenetics followed by age then circulating blast count
See auer rods in what type of leukemia
AML
what is tx for AML
remission induction chemo (50-80% achieve remission), followed by consolidation therapy to reduce relapse risk: chemo or BM transplant
Most common childhood leukemia
ALL
Typical age of ALL
2-4 years old
What very bad thing do you want to prevent in ALL
CNS leukemia
Tx of ALL
remission induction chemo, consolidation, CNS prophylaxis, maintenance therapy. BM transplant usually used for relapse
Philadelphia chromosome is cytogenetic marker for
CML
Philadelphia chromosome is a reciprocal translocation b/t what 2 chromosomes & created new fusion gene of
t(9;22), bcr/abl
What causes CML
new fusion gene bcr/abl product
tx of CML
palliative-alpha interferon, hydroxyurea or busulfan
curative-BM transplant; unknown-imatinib mesylate (Gleevec)
A single specific mutation necessary & significant for malignancy transformation (unusual in human cancers)
CML
Most common leukemia in western world
CLL
accumulation disease of morphologically mature but functionally abnormal lymphocytes
CLL
see smudge cells w/ what
CLL
only leukemia not associaed w/ radiation exposure
CLL
What is staging of CLL
low risk (avg survival 10-20 yrs)
intermed (3-10 yrs)
high risk (< 3yrs)
What is age like in CLL
a disease of aging, rare before 50
Tx of CLL
supportive care; chemo only for high risk & some intermed: chlorambucil, fludarabine (palliative). BM transplantation is experimental
Hairy cell leukemia is a related disorder of
CLL
What type of staging is used for Hodgkin's disease
Ann Arbor staging
Which stage is the following for Hodgkin's dz:

Involved lymph node regions (includes spleen) on both sides of diaphragm
Stage III
Which stage is the following for Hodgkin's dz:

Confined to single lymph node group on one side of diaphragm
Stage I
Which stage is the following for Hodgkin's dz:

Involvement of 2 or more lymph node regions on one side of diaphragm
Stage II
Which stage is the following for Hodgkin's dz:

Disseminated disease w/ involvement of extranodal tissue or organ(s)
Stage IV
Reed-Sternberg Cell is associated with
Hodgkin's disease
What disease has a bimodal age distribution and what are the peaks
Hodgkin's disease
20-30 & 55+ years old
Radiation therapy is used for what stages in Hodgkin's dz
IA, IIA, & some IIIA
Other than radiation therapy, what is used in all other stages of Hodgkin's dz
Chemotherapy, some pts receive both
What tx is used for systemic relapse in Hodgkin's dz
high dose therapy w/ autologous marrow transplantation
Large group of neoplastic diseases arising in lymphoid tissue
Non-Hodgkin's lymphoma
Classify Non Hodgkin's lymphoma
A,B,C (low grade)-long survival
D,E,F,G (intermediate grade)
H,I,J (high grade)
Non-hemolytic reaction to leukocyte Ags, or more rarely to plasma protein components. Very common in heavily transfused pts
febrile transfusion reactions
for tx of symptomatic anemia; increases oxygen carrying capacity
PRBC's
WBCs removed by in-line filtration to prevent febrile reactions, HLA sensitization, & transmission of CMV
Leukocyte-depleted PRBCs
platelet concentrate from single donor obtained by apheresis.
pheresis platelets
used to provide platelets for correction of thrombocytopenia or platelet function defect (aspirin)
Platelet-rich plasma/platelet concentrate
provides stabile clotting factors, mainly factor VIII & fibrinogen, in small volume
cryoprecipitate
This is used to rapidly correct clotting factor deficiency; large volume limits amount that can be given
fresh frozen plasma
used to preserve rare blood types & to remove plasma proteins before transfusion to sensitive patients
frozen, deglycerolized RBCs
pheresis platelets from donors lacking HLA Ags to which recipient has Abs
HLA-screend platelets
pheresis platelets from donors of known HLA type matched to recipient
HLA-matched platelets