Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
122 Cards in this Set
- Front
- Back
|
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
|
