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Pathology-Anemias I &II


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Decreased hemoglobin level resulting in decreased oxygen-carrying capacity of the blood
Clinical features of SEVERE anemia
Spoon shaped and brittle fingernails
nail bed missing half-moon shape
Brittle Hair
Fatigue, malaise on MILD exertion
hypoxic tissue damage
3 ways to classify anemias
Size of RBC's
Blood loss
Mechanisms that cause anemia
Blood loss
Impaired production
Increasd destruction
Size Classifications of RBCs
Normocytic MCV 80-100 (can still be anemic)
Microcytic MCV<80
Macrocytic MCV>100
Types of blood Loss
Chronic->GI, gyn, gross
Causes of impared RBC Production
Stem Cell Failure
Dismaturation of Erythroblasts
Defective DNA Synethesis
Defective Hgb Synhesis
Defective Heme sythesis
Defective globin synthesis
Causes of Stem Cell failure Anemia
Aplastic Anemia
Pure Red cell aplasia
Anemia of renal failure
Anemia of endocrine disorders
Causes of Defective DNA Synthesis Anemia
B12 deficiency
folic acid deficiency
folic acid antagonists
cengenital megaloblastic anemias
Variation in size of RBC's

Seen in B12 and Folate deficiency, among others
Oval shaped RBC's

Seen in B12 and Folate deficiency, among others
Characteristics of b12 and Folate deficiency
Cause DNA synthesis problems
Hypersegmented Neutrophils
Anisocytosis and macroovalocytosis
immature RBC forms in PB
Increased reticulocyte count
Hypercellular BM
RBC in peripheral blood with RNA still inside (immature form)
Pernicious Anemia
B12 deficicency
B 12 disease characteristics
Insidious onset
AB to intrinsic factor
neuro abnormalities (weakness/nubmness)
rare in children
B12 causes
intestinal malabsorption
dietary deficiency (RARE)
chronic lush
Beefy red tongue inflammation seen in pernicious anemia (what's deficient in pernicious anemia?)
Intrinsic Factor
-Secreted in the stomach
-Aids in absorption of B12 in the intestines
-Deficient after gastrectomy->b12 deficiency
Causes of Folate Deficiency
Inadequate Diet, Intestinal malabsorption, increased requirments (pregnancy, infancy), dialysis, Antagonists (ex Methotrexate->Chemotherapy Drug
Megaloblastic anemia
Looks like big RBC's, small rbc's, different sizes of RBC's and hypersegmented neutrophils
Most common nutritional disorder in children
Iron deficient anemia
Causes of Iron deficient anemia
Diet, chronic blood loss
Stages of Iron deficiency
Macrophages depleted of stored Iron
-plasma ferritin levels drop
-Serum Iron decreases, compensatory increas in transferrin
-Heme not forming so RBC free Protoporphyrin increases
Iron Deficient anemia looks like
Tiny RBC's with increased central pallor (more clear space in the center)
Sideroblastic Anemia
Associated with Myelodysplastic Syndromes, Ineffective Erythropoiesis in BM, Increased Iron stores, Lots of Fe+ in mitos, increased Iron, Increased Ferritin
Sideroblastic Anemia looks like
funky red/blue granule looking things in the rbc's The iron overload stains
Characteristics of hemolytic anemias
-Decreased lifespan of RBCs
-Accumulation of Hgb breakdown products
-increased marrow erythropoeisis
Types of hemolysis
Causes of intravascular hemolytic anemia
-Mechanical Injury (like a mechanical valve)
-Complement Fixation
-Exogenous Toxic Factors
Characteristics of intravascular hemolytic anemia
inc LDH
dec haptoglobin
hgb in the urine
Hgb outside the rbc's in the blood
Iron in the blood
Causes of extravascular hemolytic anemia
Injured cells are destroyed by mononuclear phagocyte syestem
Characteristics of extravascular hemolytic anemia
anemia, jaundice, inc LDH, SPLENOMEGALY

rbc's are handled in the spleen
Types of intrinsic red cell abnormalities that cause hemolytic anemia
Membrane disorders (hereditary or aqcuired)
enzyme defects
hgb synthesis problems
Types of hereditary membrane disorders that caus hemolysis
Red Cell enzyme defects that cause hemolysis
Hereditary G6PD deficiency-A--blacks, mild hemolysis
Hereditary G6PD deficiency-Mediterranean-More severe hemolysis


Glucose-6-phosphatase dehydrogenase
The G6PD enzyme catalyzes the oxidation of glucose-6-phosphate to 6-phosphogluconate while concomitantly reducing the oxidized form of nicotinamide adenine dinucleotide phosphate (NADP+) to nicotinamide adenine dinucleotide phosphate (NADPH). NADPH, a required cofactor in many biosynthetic reactions, maintains glutathione in its reduced form. Reduced glutathione is a scavenger for reactive oxygen species, so, without g6pd, you have less scavenging for reactive oxygen species and more cell damage

(sorry guys =)
Spherocytosis looks like
Big ball RBC's with no central pallor
Elliptocytosis looks like
Hotdog RBC's or bacteria or something
G6PD deficiency looks like
Heinz Bodies-Purple spots in RBC's

Poikilocytosis (Weird shaPed rbc's) d/t denatured Hgb from reactive oxygen species binds to the cell membrane. Spleen takes bites out the cells to try to fix them-"bite cells".

They look funky
Hemoglobin S
Sickle cell trait
Sickle Cell disease

Point mutation that replaces a glu with a val
Hgb S sickle cell trait factOIDS
8% of black americans
protects against malaria infection
30% heterozygosity in endemic areas
Normally asymptomatic
Characteristics of Sickle Cell Anemia
severe, chronic,hemolytic anemia
96% Hgb S, less severe anemia with Hgb C or D
Deoxygenation causes sickling
Treatment of Sickling crisis
Sickling crisis
Irreversibly sickled cells sequesterd and destroyed in spleen (extravascular hemolysis)
Aplastic Crisis
Overworked BM shuts down in sickling crisis
Sequestration Crisis
Too many sickled RBC's in the spleen cause splenomegaly in children
Features of Sickle Cell Anemia
-Need for frequent transfusions->Hemosiderosis
-bone marrow hypercellularity
-vascular infarctions
-inc susceptability ot blood borne infections due to spleen prob
-prone to S. Pneumoniae and H. Influenzae
-Septicemia and meningitis common COD
-Vasocclusive crisis
Iron Overload from frequent transfusions
Vasocclusive crisis
-Very painful
-Acute Chest syndrome
-stroke, seizure
-heart and kidney involvement
-leg ulcers
Sickle Cell looks like
sickled cells-duh
Deficient globin synthesis is called?

-Normal globin chains but imbalance of production
1 gene deletion
α thalassemia
Silent Carrier State
2 gene deletion
α thalassemia
Alpha Thalassemia Trait
3 gene deletions
α thalassemia
Hgb H disease
4 gene deletions
α thalassemia
Hydrops Fetalis
(most severe)
Newborns with excess unpaired gamma chains (form tetramers)
Hgb Barts
Adults with excess unpaird beta chains (form tetramers)
Hgh H
Beta Thalassemia
Heterozygotes protected against malaria

most in mediterraniean, africa, SE asia

Large number of variants

often misdiagnosed as iron deficiency anemia
Types of β thalassemia variants
-Silent Carrier state
-Beta Thal Trait
-Thalassemia intermedia
-thalassemia major (Cooleys Anemia)
Thalassemias look like
-Anisocytosis (lots)
-Target Cells (red cells with inc SA to volume ratios)
-nucleated RBC's
-Masophilic stipling
-schistocytes (fragmented RBC's)
lab findings in thalassemias
inc wbc w/ left shift
normal platelet count
decreased hgb values (2-8 gm/dl)
inc serum iron and ferritin
Paroxysmal Nocturnal Hemoglobinuria
rare, acquired stem cell disorder
rbcs, grans, plts prone to complement-mediated lysis (membrane defect)
episodic lysis, worse at night
survival-10 yrs
Diagnosis of PNH
-Sucrose hemolysis test
-Hams Test
Preformed antibodies to non-self antigens
Cause transfusion reactions and hemolytic disease of newborns
Extrinsic red cell abnormalities
Antibody mediated hemolysis
-autoimmune hemolytic anemias
-paroxysmal cold hemoglobinuria
Warm Type autoimmune hemolytic anemia
60% idiopathic
Drugs, lymphoma, SLE
IgG binds at 37 degrees C
Cold Type autoimmune hemolytic anemia
Mycoplasma infection and EBV
IgM binds in cold
Ex-Raynauds syndrome
Paroxysmal Cold hemoglobinuria
Acute intermittent massive hemolysis in the cold
IgG against P-blood group antigen
Binds complement at low temp
reslting complement activation and intravascular hemolysis at body temp
biphasic antibody (donath-landsteiner ab)
associated with measles, mumps, virus, flu-like, selflimiting
types of microangipathic hemolytic anemias
DIC-Disseminated intravascular coagulopathy
HUS-Hemolytic uremic syndrome
TTP-Thrombotic thrombocytopenic pupura
Macroangipathic hemolytic anemias
mechanical trauma to rbc's sometimes caused by mechanical heart valves.

Did you hear the click in my valve?
(1) One of the most life threatening emergencies you can encounter.
(2) Situation of inappropriate coagulation where all of the clotting factors are consumed, and therefore you bleed because nothing can clot.
(3) Begins with an event that triggers widespread clotting and the formation of microthrombi.
(4) Causes include
(a) Obstetric accidents
(b) Retained dead fetus
(c) Overwhelming sepsis
(d) Trauma
(e) Massive hemorrhaging
(1) Simultaneous triad of hemolytic anemia, thrombocytopenia, and acute renal failure
(2) Uncommon
(3) Occurs primarily in children
(a) 2 types in children
(i) after a diarrheal event
1. frequently an E. coli infection after the child has ingested contaminated meat.
2. can be deadly
(ii) after a non-diarrheal event
(1) Fever, hemolytic anemia, thrombocytopenia (decreased platelets), neurological and renal abnormalities
(2) Aggregations of platelets that obstruct the arterioles and capillaries in the brain and other organs.
(3) Usually occurs of an infection.
(4) Usually seen in adults, ages 20-50.
(5) Usually not fatal.
Hemolytic anemia in infections
malaria and babesiosis

rupture and hemolysis of cell by organism

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