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68 Cards in this Set

  • Front
  • Back
Difference b/w anti AB antibodies and anti Rh antibodies?
Rh antibodies are IgG (cross placenta)
AB antibodies are IgM (do not cross placenta)
Macrovalocytes seen in?
Megaloblastic anemia (also hypersegmented PMN's), and marrow failure
Helmet cells, schistocytes seen in?
DIC, TTP/HUS, traumatic hemolysis
Bite cell seen in?
G6PD deficiency
Teardrop cell seen in?
Myeloid metaplasia w/myelofibrosis
Acanthocytes (spur cells) seen in?
Spiny appearance in liver disease and abetalipoproteinemia
Target cell seen in?
HbC disease
Liver disease
Burr cells seen in?
Basophilic stippling seen in?
Anemias of chronic disease
Iron deficiency
Lead poisoning
Heinz bodies
(a) etiology
(b) seen in?
(a) oxidation of iron from ferrous to ferric leads to denatured Hgb precipitation and damage to RBC membrane; forms bite cells
(b) alpha thalassemia, G6PD deficiency
Howell Jolly bodies
(a) etiology
(b) seen in?
(a) basophilic nuclear remnants found in RBC's
(b) hypo/asplenic patients
Etiologies of microcytic, hypochromic anemias (MCV<80)
Iron deficiency
Lead poisoning
Some sideroblastic anemias
Differential feature b/w iron deficiency and thalassemia hypochromic, microcytic anemias
In thallassemia you have increased # of microcytes
IN iron deficiency you have decreased # of microcytes
Etiologies of macrocytic anemias (MCV>100)
Megabloblastic (vitB12/folate deficiency)
Drugs that block DNA synthesis (sulfa drugs, phenytoin, AZT)
Decr serum haptoglobin
Incr serum LDH indicate?
RBC hemolysis
Abdominal pain
Pink urine
Psychological disturbances
Precipitated by drugs
Lead poison effect on heme synthesis
(a) enzyme(s) inhibited
(b) accumulated substrate in urine
(a) ferrocheletase; ALA dehydratase
(b) coproporphyrin & ALA
Acute intermittent porphyria
(a) enzyme inhibited
(b) accumulated substrate in urine
(a) uroporphyrinogen I sunthase
(b) prophobilinogen and gamma ALA
Porphyria cutanea tarda
(a) enzyme inhibited
(b) accumulated substrate in urine
(a) uroporphyrinogen decarboxylase
(b) uroporphyrin
Acute intermittent porphyria presentation (inheritence)
Autosomal Dominant
Episodic expression
Abd pain
Muscle weakness
Port wine urine in some patients
NO photosensitivity
Porphyria cutanea Tarda presentation
Skin inflammation and blistering
Cirrhosis often associated
Lead poisoning presentation
Microcytic sideroblastic anemia
Basophilic stippling
HA, nausea, memory loss, abd pain, diarrhea
Lead lines in gums
Neuropathy (claw hand, wrist drop)
Primary iron storage protein of body
Transport iron in blood
Binds free heme in blood
Iron deficiency
(a) serum iron
(b) transferrin/RIBC (indirectly measures transferrin)
(c) ferritin
(d) % transferrin sat (serum Fe/TIBC)
(a) serum iron: low (primary)
(b) transferrin/TIBC (indirectly measures transferrin): incr
(c) ferritin: low
(d) % transferrin sat (serum Fe/TIBC): very low
Chronic disease
(a) serum iron
(b) transferrin/TIBC (indirectly measures transferrin)
(c) ferritin
(d) % transferrin sat (serum Fe/TIBC)
(a) serum iron: low
(b) transferrin/TIBC (indirectly measures transferrin): low
(c) ferritin: high (primarily)
(d) % transferrin sat (serum Fe/TIBC): nml
(a) serum iron
(b) transferrin/TIBC (indirectly measures transferrin)
(c) ferritin
(d) % transferrin sat (serum Fe/TIBC)
(a) serum iron: high (primary)
(b) transferrin/TIBC (indirectly measures transferrin): low
(c) ferritin: high
(d) % transferrin sat (serum Fe/TIBC): very high
Pregnancy/OCP use
(a) serum iron
(b) transferrin/TIBC (indirectly measures transferrin)
(c) ferritin
(d) % transferrin sat (serum Fe/TIBC)
(a) serum iron: nml
(b) transferrin/TIBC (indirectly measures transferrin): high (primary)
(c) ferritin: nml
(d) % transferrin sat (serum Fe/TIBC): low
Aplastic anemia
Due to failure or destruction of multipotent myeloid stem cells
Etiologies of aplastic anemia
Alkylating agents
Viruses (B19, EBV, HIV)
Fanconie's anemia (inherited defect in DNA repair)
May follow acute heptatitis
Symptoms of aplastic anemia
Mucosal bleeding
Pathologic features of aplastic anemia
Pancytopenia w/normal cell morphology, hypocellular bone marrow w/fatty infiltration. Diagnose with bone marrow biopsy
Treatment of aplastic anemia
Withdrawal of offending agent.
Immunesuppressive regiments
Allogeneic BMT
RBC and platelet transfusion
Myelophthisic anemia
Displacement of hematopoietic bone marrow by infiltrating tumor
Mutation in sickle cell anemia
Valine fro glutaminc acid in position 6 of beta chain of Hgb
Sickel trait manifestations
40% have a sickle crisis in extreme conditions (low oxygen or dehydration)
Sickle prep
Blood sample treated with a reducing agent (sickled cells may be seen)
Diagnosis of sickle cell anemia
Hgb electrophoresis
Advantage of heterozygotes (sickle trait)
Protective against falciparum malaria
Complications of sickle cell anemia patients
Aplastic crisis (parvovirus B19)
Incr risk of encapsulated organism
Salmonella osteomyelitis
Painful crisis
Renal papillary necrosis
Splenic sequestration
Therapies for sickle cell anemia
Hydroxyurea (incr HgbF)
Bone marrow transplant
"crew cut" skull on x ray seen in? why?
Sickle cell anemia and thallasemia
Due to marrow expansion from incr erythropoiesis
HbC disease
Different beta chain mutation; patients w/HbC or HbSC have a milder disease than HbSS patients
Defect in alpha thalassemia
Defect in 1 to 4 alpha globin genes
Alpha globin is underproduced w/nocompensatory incr in any of the other chains
1 deleted alpha globin chain mutation
Silent carrier
2 deleted alpha globin chain mutation
Alpha thal trait
3 deleted alpha globin chain mutation
HbH disease; hemolysis and anemia
4 deleted alpha globin chain mutation
Hydrops fetalis (bart Hb); intrauterine death
Alpha thalassemia is prevalent where geographically?
Asia and africa
Defect and result in beta thalassemia
Mutations in splicing sites and promoter sequences for beta globin gene
Excess of alpha chains causes Hgb aggregates (insoluble)
Intra and extramedullary hemolysis
Extramedullary hematopoiesis
HbS/beta thal
Mild to moderate sickle disease dependeing on amnt of beta globin production
Treatment of beta thal major
Severe anemia requiring blood transfussions
Complications of beta thal major
Heart failure due to secondary hemochromatosis
Hemolytic anemia: hemoglobinuria indicates?
Intravascular hemolysis
Hemolytic anemia: jaundice indicates?
Extravascular hemolysis
Warm agglutinin hemolytic anemia
(a) mechanism
(b) etiologies
(a) IgG autoimmune hemolytic anemia; accelerated RBC destruction in liver Kupffer cells and spleen)
(b) SLE, CLL, certain drugs (alpha methyl dopa)
Cold agglutinin hemolytic anemia
(a) mechanism
(b) etiologies
(a) acute anemia triggered by cold; IgM antibodies against RBC
(b) mycoplasma, mononucleosis, idiopathic, lymphoma
Hereditary spherocytosis defect
Ankyrin, band 3.1 or spectrin defectl; cause RBCs to be less pliable and vulnerable to destruction in the spleen
MCHC and RDW in hereditary spherocytosis
Symptoms of hereditary spherocytosis
Anemia, jaundice, splenomegaly, cholelithiasis
Treatment of hereditary spherocytosis
Presplenectomy smear for hereditary spherocytosis
Cells lacking central pallor; reticulocytosis
Postsplenectomy smear
More spherocytes and Howel Jowel bodies
Paroxysmal nocturnal hemoglobinuria cause (defect)
Intravascular hemolysis due to memraben defect; incr sensitivity of RBC to lytic activity of complemement (impaired synth of GPI anchor/decay accelerating factor in RBC membrane).
See hemosiderin in urine
G6PD deficiency defect (inheritence)
XL defect of hexose monophsophate shunt enzyme
Decreased regeneration of NADPH (and thus glutathione)
Older cells unable to tolerate oxidative stress
Cause of G6PD related anemia
Drugs (sulfa, quinine, nitrofurantoin)
Infections (particularly viral)
Certain foods (fava beans)
Smear in G6PD deficiency
Reticulocytosis and Heinz bodies (Hgb degradation products)