|
 normal RBC shape | bioconcave |
| autoimmune hemolysis/ hereditary spherocytosis | spherocytes |
| hereditary elliptocytosis | elliptoctye |
| marrow failure, hypersegmented PMN, megaloblastic anemia | macro-ovalocyte |
| helmet cell/schistocyte/little triangles | traumatic hemolysis, TTP, DIC, HUS, MAHA |
| sickle cell anemia | sickle cell |
| bite cell | G6PD deficiency |
| myeloid metaplasia with myelofibrosis | tear drop cell |
| acanthocyte/spur cell (extreme remodeled acanthocyte) | spiny appearance in liver disease and abetalipoproteinemia; chorea acanthocytosis, McLeod syndrome |
| target cell (HALT to the target) | HbC, asplenia, liver disease, thalassemia |
| burr cell/echinocytes | TTP/HUS, old blood artifact |
| describe acanthocyte | Acanthocytes are cells with five to ten irregular, blunt, finger-like projections. The projections vary in width, length, and surface distribution ( |
| describe echinocytes | echinocytes, another morphologic variation of the erythrocyte that occurs in an alkaline pH or with certain diseases or disorders; Echinocytes have multiple, small, delicate regular-shaped spines distributed evenly around the cell membrane and are indistinguishable from artifactually crenated cells |
| differential for echinocytes | snake bite evenomation; Echinocytosis has been observed in lymphosarcoma, pyruvate kinase (PK) deficiency, furosemide, erythrocyte dehydration, uremia, doxorubicin treatment, and glomerulonephritis. |
| differential for acanthocytes | hepatic disease, hemangiosarcoma, cholesterol rich diet, abetalipoproteinemia |
| compare acanthocyte to echinocyte | although often confused with acanthocytes, the projections of the red cell membrane are smaller and much more uniform in shape and distribution in echinocytes; Echinocytes are often found as artifacts on blood smears. They can be produced in vitro by incubation at high pH or in the presence of high calcium concentrations, exposure to glass surfaces, reduced albumin concentrations, and after prolonged storage |
| McLeod Syndrome | It is caused by a variety of recessively-inherited mutations in the XK gene on the X chromosome. The gene is responsible for producing a specific protein (Kell antigen) on the red blood cell surface; patients usually begin to notice symptoms in their 50s and the course is usually slowly progressive. Common features include peripheral neuropathy, cardiomyopathy and hemolytic anemia. Other features include limb chorea, facial tics, other oral movements (lip and tongue biting), seizures, a late-onset dementia and behavioral changes. |
| chorea acanthocytosis | an autosomal recessive disorder, directs structural proteins in red blood cells. When a patient's blood is viewed under a microscope, some of the red blood cells appear thorny; epilepsy, behaviour changes, muscle degeneration, and neuronal degradation similar to Huntington's Disease. The average age of onset of symptoms is 35 years |
| basophilic stippling | TAIL: Thalassemia, anemia of chronic disease, iron deficiency, lead poisoning |
| howell jolly bodies | seen in patients with hyposplenia or asplenia, basophilic nuclear remnants in RBCs |
| Heinz bodies | oxidation of ferrous (Fe2+) to ferric (fe3+) leads to denatured Hb precipitation and damage to RBC membrane; leads to formation of bite cells; seen in alpha-thalassemia and G6PD deficiency |
| 9:22 translocation | pihladelphia chromosome seen in chronic myelogenous leukemia; produces bcr-abl fusion protein constitutively active tyrosine kinase that promotes cell overgrowth |
| gleevec/imatinib | tyrosine kinase inhibitor to treat CML |
| hereditary spherocytosis | spherocytes of red blood cells, mutations in spectrin, ankyrin, band 3, or protein 4.2. rbcs are not as flexible so when they go via sinusoids of spleen, they are trapped there and destroyed. splenectomy is best option for this hemolytic anemia. |
| when do you see eosinophilia | neoplasia, asthma, allergies, collagen vascular disease or parasitic infection. |
| major basic protein | The protein encoded by this gene is the predominant constituent of the crystalline core of the eosinophil granule; This protein may be involved in antiparasitic defense mechanisms as a cytotoxin and helminthotoxin, and in immune hypersensitivity reactions. It is directly implicated in epithelial cell damage, exfoliation, and bronchospasm in allergic diseases |
| Myeloperoxidase (MPO) | abundantly present in neutrophil granulocytes (a subtype )of white blood cells). It is a lysosomal protein stored in azurophilic granules of the neutrophil. MPO has a heme pigment, which causes its green color in secretions rich in neutrophils, such as pus and some forms of mucus; MPO produces hypochlorous acid (HOCl) from hydrogen peroxide (H2O2) and chloride anion (Cl-) (or the equivalent from a non-chlorine halide) during the neutrophil's respiratory burst. It requires heme as a cofactor. Furthermore, it oxidizes tyrosine to tyrosyl radical using hydrogen peroxide as oxidizing age |
| describe asthma | Asthma exists in two states: the steady-state of chronic asthma, and the acute state of an acute asthma exacerbation. The symptoms are different depending on what state the patient is in; Common symptoms of asthma in a steady-state include: nighttime coughing, shortness of breath with exertion but no dyspnea at rest, a chronic 'throat-clearing' type cough, and complaints of a tight feeling in the chest |
| treatment for gout | allopurinol, colchicine, probenacid |
| erlichiosis | erlichia chaffeensis, a member of Rickettsia; carried by dog tick; forms characteristic berry like cytoplasmic inclusions in macrophages/neutrophils; treat with doxycycline |
| what fungal infection does erlichia make you susceptible to | candidiasis by candida albicans |
| trisomy 18 | edward's syndrome |
| trisomy 13 | patau syndrome |
| malignancies associated with down's syndrome | epicanthal folds, duodenal atresia, congenital heart disease, Alzheimer's, ALL |
| symptoms of lead poisoning | anorexia, hyperirritability, altered sleep patterns, decreased play, abdominal pain, vomitting, constipating, ataxia, coma, seizure, encephalopathy; defective aminolevulinic acid dehydratase, lead induced porphyria |
| gaucher's disease | deficiency in beta glucocerebrosidase, leading to accumulation of glucocerebroside in reticuloendothelial system; cause organomegaly and infiltration of bone marrow, anemia, thrombocytopenia, erlenymeyer flask appearance of distal femur |
| problem with acetaminophen | depletion of glutathione; |
| hexosaminidase A deficiency | Tay Sach's , see accumulation of gangliosides , macrocephaly, seizures, cherry red spots in macula |
| etoposide | topoisomerase inhibitor; used as anticancer drug |
| vincristine | alkaloid, mitotic inhibitor, binds microtubules and disrupts metaphase of mitoses; used as anticancer drug |
| bleomycin | antibiotic used for testicular and squamous cell carcinoma, binds DNa and introduces strand breaks; prevents thymidine synthesis |
| 5-fluoro uracil | used as anticancer drug, blocks thymidine and prevents DNA synthesis |
| diagnosis of DVT vs pulmonary embolism | use venography,ultra sound, impedance plethysmography OR angiography/ventilation perfusion or CT scan |
| 20-50% of patients with HIT will develop thrombosis, True or False | true; you'd think low platelet count will be normal clotting, but no. antibody against PF4-heparin complex mediated clotting is induced; you tissue necrosis |
| Trousseau syndrome (associated with pancreatitis, adenocarcinoma of liver, brain venous arterial clots) | mucin that activates clots in certain cancers that is associated with venous thrombosis[1] and hypercoagulability; the blood may spontaneously form clots in the portal vessels, the deep veins of the extremities (such as the leg), or the superficial veins anywhere on the body. These clots present as visibly swollen blood vessels (vasculitis), especially the veins, or as intermittent pain in the affected areas; marantic/non bacterial thrombotic endocarditis |
| Budd-Chiari syndrome(associated with myeloproliferative disorders) | clinical picture caused by occlusion of the hepatic veins. It presents with the classical triad of abdominal pain, ascites and hepatomegaly; elevated liver enzymes, and eventual encephalopathy |
| what is haptoglobin | n blood plasma, haptoglobin binds free hemoglobin (Hb) released from erythrocytes with high affinity and thereby inhibits its oxidative activity. The haptoglobin-hemoglobin complex will then be removed by the reticuloendothelial system (mostly the spleen). In clinical settings, the haptoglobin assay is used to screen for and monitor intravascular hemolytic anemia. |
| how is haptoglobin useful to distinguish intra vs extra vascular hemolysis | In intravascular hemolysis free hemoglobin will be released into circulation and hence haptoglobulin will bind the Hb. This causes a decline in Hp levels. Conversely, in extravascular hemolysis the reticuloendothelial system, especially splenic monocytes, phagocytose the erythrocytes and hemoglobin is not released into circulation and hence haptoglobulin levels are normal |
| elliptocytosis | associated with mutations in spectrin and band 4.1 |
| what is the problem with propyl thiouracil used for hyperthyroidism | Propylthiouracil causes drug-induced agranulocytosis. Although it resolves following discontinuation of the medication, the acute presentation of this complication can be associated with mortality as high as 10% |