Microcytic Anemia Flashcards
Fe Absorption Location/State
Duodenum and Fe2+. So gastectomy causes bad absorption bc acidic keeps Fe in Fe2+ state.
Fe Deficiency 6 Lab Values
Decreased ferritin, increased TIBC, decrease serum Fe, decreased %sat
Also increased RDW because initially tries to make normocytic then makes smaller
Also increased free erythrocyte protoporphyrin bc no Fe to bind
Plummer Vinson Syndrome
Fe deficiency anemia with esophageal web and atrophic glossitis
Anemia of Chronic Disease (what it is/mech/reason, treatment
Production of hepcidin, and acute phase reactant. Trying to limit amount of Fe bacteria have access to, so sequesters in macrophages/storage sites and decreases EPO production (CKD also obviously causes)
So exogenous EPO might help, and treating underlying cause
Anemia of Chronic Disease 5 Lab Values
Normocytic first too
Increased ferritin, decreased TIBC, decreased serum Fe, decreased % saturation
Also increased free erythrocyte protoporphyrin bc no heme to attach
Sideroblastic Anemia (what it is, why you get smear findings)
Anemia due to defective protoporphyrin synthesis. Iron enters mt to form heme, but if protoporphyrin deficient Fe remains trapped and the Fe-laden mitochondria form a ring around the nucleus of erythroid precursors, ringed sideroblasts
4 Causes of Sideroblastic Anemia
Congenital, most often defect of ALA Synthase (ALAS, rate limiting)
Alcoholism - mt poison
Lead poisoning - inhibits FERROCHELATASE and ALA DEHYDRATASE
Vitamin B6 Deficiency - req’d cofactor of ALAS, most often seen from isoniazid
4 Lab Values of Sideroblastic Anemia
Fe overload so
High ferritin, low TIBC, high serum Fe, high % saturation
Pregnancy 2 Fe Lab Values
High TIBC and low % saturation
alpha-Thalassemia by #of Alleles deleted 1-4`
1 - asymptommatic
2 - Trait. Mild with increased risk in offspring. cis prevalent in Asians, trans in Africans
3 - HbH disease, severe anemia. Get Beta tetramers (HbH) because very little alpha
4 - lethal in utero, hydrops fetalis. Get Hb Bart (gamma tetramers) because no alpha
Beta Thalassemia Cause/Demographic
Point mutations in splice sites and promoter sequences of Beta globin genes
Mediterranean populations
Beta Thalassemia Minor (what it is, dx, also another problematic condition when concurrent)
Heterozygote so just less of Beta globin. Usually asymptomatic so dx by increased HbA2 (alpha2delta2) on electrophoresis
Heterozygote with sickle cell can cause moderate disease
Beta Thalassemia Major (when it presents, what happens/presentation, big risk, treatment/complication, smear, electrophoresis)
Presents a few months after birth because HbF protective
alpha2 tetramers aggregate damaging RBCs/ineffective erythropoeisis/splenic breakdown
Massive marrow expansion causing crew cut skull and chipmunk facies/extramedullary hematopoeisis so hepatosplenomegaly
Parvovirus can cause aplastic crisis
Treat with blood transfusion, can cause secondary hemochromatosis
Smear shows microcytic, hypochromic RBCs and target cells, anisocytosis, poikilocytosis, schistocytes, etc
Little or no HbA and increased HbA2 and HbF
4 Diseases Causing Target Cells
HALT - HbC disease, Asplenia, Liver disease, Thalassemia
