lab 1 Flashcards by connor prusz

CBC
Decreased RBC
decreased hgb
MCV normal
Slide review reveals nucleated (young) RBCs
Retic count is ordered additionally to CBC
Supravital stain

Acute blood loss anemia

How well did you know this?

Not at all

Perfectly

Due to trauma, surgery, GI bleeding

Normocytic, normochromic anemia with increased reticulocytes

Acute blood loss anemia

How well did you know this?

Not at all

Perfectly

Microcytic, hypochromic anemia

Iron deficiency anemia

How well did you know this?

Not at all

Perfectly

CBC
Decreased RBC
Decreased HGB
Low MCV
Add- on testing? Iron studies

Iron deficiency anemia

How well did you know this?

Not at all

Perfectly

Microcytic, hypochromic anemia
Usually a normal RBC count relative to level of anemia
Target cells, basophilic stippling often present, normal RDW
Definitive diagnosis with hemoglobin electrophoresis

Thallasemia

How well did you know this?

Not at all

Perfectly

Thallasemias are a group of hereditary anemias where there is deficient production of alpha or beta hgb.
Alpha thallasemia major, alpha thallasemia minor
Beta thallasemia major, beta thallasemia minor
Patients with life-long microcytic anemia
unresponsive to Fe therapy

Thallasemia

How well did you know this?

Not at all

Perfectly

Worse morphology with normal iron

Thallasemia

How well did you know this?

Not at all

Perfectly

Spherocytes=

RBCs lacking central pallor

How well did you know this?

Not at all

Perfectly

How to confirm Spherocytes?

osmotic fragility test

How well did you know this?

Not at all

Perfectly

> 25 % of RBCs with elliptocyte/ovalocyte morphology to distinguish from other conditions

Hereditary elliptocytosis

How well did you know this?

Not at all

Perfectly

Ususally normocytic, normochromic but may be microcytic

Lab findings: Low reticulocyte count, normal to increased ferritin and iron stores, decreased serum iron.

Anemia of chronic disease

How well did you know this?

Not at all

Perfectly

Increased reticulocyte count

High serum bilirubin levels from increased RBC destruction

Hemolytic anemia

How well did you know this?

Not at all

Perfectly

: hereditary hemoglobinopathies, G6PD deficiency, sickle cell

Intrinsic

How well did you know this?

Not at all

Perfectly

autoimmune destruction, heart valves, burns

Extrinsic

How well did you know this?

Not at all

Perfectly

Cold induced Hemolytic

IgM mediated

usually only a problem for laboratory testing (blood banking)

How well did you know this?

Not at all

Perfectly

Warm Hemolytic

IgG mediated: extravascular hemolysis by splenic macrophages
Majority of AIHA, Reacts at body temp
Peripheral blood: NRBCs, schistocytes, spherocytes, increased retics
Direct antiglobulin test (DAT)
Patients serum reacts with screening cells

How well did you know this?

Not at all

Perfectly

Hemolytic disease of newborn

Determine amount of fetomaternal hemorrhage with Kleihaour-Betke test

How well did you know this?

Not at all

Perfectly

Kleihaour-Betke test

Hemolytic disease of newborn

Determine amount of fetomaternal hemorrhage with

How well did you know this?

Not at all

Perfectly

Vasculature capable of shredding RBCs via formation of fibrin/clot within vessels
Labs: schistocytes on peripheral smear
High LDH and bilirubin
DIC: disseminated intravascular coagulation
TTP: thrombotic thrombocytopenic purpura
HELLP: hemolysis, elevated liver enzymes, low platelets

Microangionpathic hemolytic anemia

How well did you know this?

Not at all

Perfectly

Most common RBC enzyme disorder

Requires Requires supravital stain for visualization

G6PD deficiency

How well did you know this?

Not at all

Perfectly

Heinz bodies removed by spleen producing

bite cells

How well did you know this?

Not at all

Perfectly

G6PD deficiency def. Diagnosis

Definitive diagnosis by demonstrating decreased enzyme activity or by identifying genetic abnormality with PCR

How well did you know this?

Not at all

Perfectly

Megaloblastic anemia: abnormal cell development
Nuclear-cytoplasmic synchrony- defects in all cell types
Macrocytic anemia (MCV >100)
Macroovalocytes, hypersegmented PMNs, macroplatelets

Study These Flashcards

Folate deficiency

Megaloblastic
Macrocytic anemia
Serum b12 level

Study These Flashcards

B12 deficinency

Microcytic hypochromic anemia Basophilic stippling of RBCs (precipitate of RNA, mitochondria) S/Sx: abdominal pain, cognitive impairment, irritability Acute onset: vomiting, seizures, AMS

Lead poisoning

Increased RBC | Hgb >18.5 g/dL in males, Hbg > 16.5 in females

erythrocytosis

erythrocytosis Dx:

must directly measure RBC mass and perform bone marrow bx | Tx: therapeutic phlebotomy

Measured in lab by partial thromboplastin time (PTT) | Monitor herparin/lovenox therapy

Intrinsic pathway

VII and tissue factor Measured in lab by prothrombin time (PT/INR) Monitor Coumadin therapy

Extrinsic pathway

I, II, V, X

Common pathway: thrombin activates fibrinogen to fibrin

mutation making factor V resistant to protein C degradation causing hypercoagulable state

Factor V Leiden:

Antithrombin | Anticoagulant properties greatly increased by

heparin

fibrinolysis Major enzyme is

palsmin

Fibrinogen cleaves clot into specific fibrin degredation products (FDPs):

d-dimer

Measures PLT function in vivo- measures amount of time for patient to stop bleeding from a superficial cut

Bleeding time | Normal: 1-9min

Test PLT ability to aggregate in vitro in presence of different reagents- identify qualitative PLT disorders

Platelet Aggregation test

Measures clot formation by extrinsic pathway | INR: algorithm to reduce variability in PT between labs

PT: prothrombin time

Measures clot formation via intrinsic pathway

PTT: partial thromboplastin time

Measures conversion of fibrinogen to fibrin

Thrombin time

Factor VIII deficiency Dx: prolonged PTT w/ normal PT Factor assay will show decreased factor VIII

Hemophilia A

Deficiency of factor IX | Prolonged PTT w/ normal PT

Hemophilia B

Needed by hepatic cells to produce factors II, VII, IX, X

Vitamin K deficiency

MC d/t infection (10-20% incidence in gram neg sepsis)

Disseminated intravascular coagulation:DIC

Acute: sudden onset severe bleeding HELLP: hemolysis, elevated liver enzymes, low PLTs in peripartum women

Disseminated intravascular coagulation:DIC

Thrombocytopenia, PT & PTT ↑, fibrinogen ↓, D-dimer + | Schistocytes on peripheral smear

Disseminated intravascular coagulation:DIC

Decreased PLTs on CBC, normal coag studies

Immune thrombocytopenic purpura (ITP)

PLT count decrease by >50% after exposure to heparin is diagnostic

Heparin-induced thrombocytopenia

Thrombocytopenia within 5-10 days of heparin tx | Less common with LMWH

Heparin-induced thrombocytopenia

Persistently elevated PLT count with increased megakaryocytes in BM

Essential thrombocythemia

Most common inherited bleeding disorder

Von Willebrand Disease

Ristocetin cofactor assay: assess PLT ability to aggregate in presence of ristocetin Early sx: easy bleeding/bruising in childhood.

Von Willebrand Disease

MC inherited cause of hypercoagulability (3% of population)

Factor V Leiden

Point mutation in factor V, making it resistant to degradation by protein C

Factor V Leiden Testing clot based: inability of activated protein C (APC) to prolong clotting time Confirmatory test with PCR (polymerase chain reaction) to look for specific abnormality in patient DNA

Labs: same as microangiopathic hemolytic anemia Schistocytes, reticulocytes, LDH increased, bili increased Tx: plasma exchange

Thrombotic thrombocytopenic purpura

Triad Thrombocytopenia with generalized purpura Microangiopathic hemolytic anmeia w/ jaundice Neuro sx: weakness, dysphasia, HA, seizures… Pentad: add fever and renal dysfunction

Thrombotic thrombocytopenic purpura

lab 1 Flashcards

(55 cards)