Heme/Onc Flashcards
A patient with a family hx of breast cancer most likely has a gene defected in what?
BRCA. increased risk of breast and ovarian cancer. plays role in gene repair and transcription
What is a good sensitive marker for bladder cancer in their malignant potential?
Involvement of muscular layer. Painless hematuria is bladder cancer.
increased activity is most likely responsible for conversion of pro-carcinogens to carcinogens
P450 microsomal monooxygenase. Metabolizes steroids, EtOH, toxins, and other foreign substances but can also convert pro-carcinogens to carcinogens.
What are the patches in mycosis fungoides called?
Proliferating CD4+ infiltrates skin. Cuse pautrier microabscesses.
What chromosome is affected in the disease that has a waxing and waning lymphadenopathy?
Follicular lymphoma - t(14;18)
In megaloblastic anemia, why should you give folate and B12 concurrently?
Def of B12 is associated with megaloblastic anemia and neuro dysfunction. Moderate improvement in hemoglobin level can be seen with just one of two treatments but treatment of cobalamin deficiency can actually worsen neuro dysfunction.
How does ondansetron work?
5-HT3 antagonist. Prevent vomiting. Blocking vagus-mediated nausea and blocking serotonin in chemo trigger zone. In GI tract, block medulla oblongata’s vomit center.
Where are 5HT3 receptor located?
In presynaptic nerve terminals of vagus nerve in GI tract and centrally in the chemoreceptor trigger zone and solitary nucleus/tract
First thing to look at with microcytic anemia?
GI bleed –> iron deficiency anemia
Why do people who have recently started warfarin can develop a rash/necrosis?
Protein C (and S) is natural anticoagulant. After starting, those can drop first and if patient is hypercoagulable to begin with (protein c defic) –> can cause hypercoagulabe state with thrombotic occlusion of microvasculative and skin necrosis
what form of cancer has risen dramatically in the last few decades for women
lung, both in mortality and incidence
If P(50) for hemoglobin went from 26mmHg to 20mmHg, what would happen?
Polycythemia - you have increased affinity for oxygen. Less oxygen at tissue level, tissue hypoxia and a result, reflex polycythemia.
An African American women with photodistributed skin rash and arthralgia with proteinuria has pancytopenia. Explain.
Person has SLE. Esp cuz she’s black. Type II hypersensitivity response, they form warm IgG Abx to RBC. AutoImm hemolysis. Spherocytosis, positive Coombs, extravascular hemolysis. Low platelets like ITP-esque. Also can get neutropenia.
What bone pathology are sickle cell patients at risk for?
Osteomyelitis. Likely salmonella, followed by Staph aureus and E coli
Are sis/TGF-alpha/ERB-B1 onco or tumor suppressor genes? If so, what do they code for?
sis - astrocytoma/osteo. ERB-B1: Lung SCC. TGFalpha-astro, HCC.
Pt has many immature cells (band forms, metamyelocytes, myelocytes) and few bands. leukcoyte alkaline phosphatase is low. Diagnosis?
CML. Leukemoid rx has normal/elevated in leukemoid rx.
Patient has thrombocytopenia with an ezcematous skin rash and recurrent URI. What infx is he at risk for?
Wiskott-Aldrich patients are at risk for encapsulated organisms: N. meningitis, H flu, STrep peumo. Later t cell defect can lead to P jiroveci and HSV. Need HLA-bone marrow transplant.
Platelet derived growth factor are found in what type of leukemia?
CML
A patient w/ hx of heavy periods and nosebleeds has a Hgb of 9.2 and MCV of 72, ferritin is low. Why?
Pt has vWF deficiency. also may have gingival/mucosal bleeding. Bleeding results in iron deficiency anemia
In hereditary spherocytosis, why is MCHC elevated?
Mild dehydration of RBC
If a person is vit B12 deficient, how do you differentiate b/w the causes?
Give radioactive B12. If normal urine levels, it’s dietary. If low, then malabsorption or pernicious anemia. Then give B12 with intrinsic factor (also low in malabsorption, esp in the ileal).
Monoclonal abx against CD21 is helpful for treating what virus?
EBV gp350 binds with CD21 normally on surface of B cells and nasopharyngeal epithelial cells.
When does HbA2 switch to HbA
During the first 6 months of life. First few weeks is all HbF, startnig at 10-12 wks of gestation.
What is the role of 2,3 DPG and ho does it relate to fetal hemoglobin?
2,3 DBG forms ionic bonds with two beta subunits of HbA after Hb is deoxygenated. HbF binds oxygen with greater affinity b/c of inability to interact with 2,3 DBP
What is probenecid used for?
Substance that increases uric acid excretion. Useful for treating gout and hyperuricemia. Effective only in pts with good renal function.
What can you do to prevent disorder that causes hyperphosphatemia, hypocalcemia, hyperkalemia, and hyperuricemia?
IV hydration and allopurinol/rasburicase can be given. Rasburicase is used to convert uric acid to allantoin, which is way more soluble. Prevent hyperuricemia and renal issues of tumor lysis syndrome.
What is denosumab for?
monoclonal ab that prevents osteoclast fx by binding to RANKL, preventing interaction with RANK (like osteoprotegerin). Decreases bone loss/fracture in people with bony mets.
What is the involved regulatory/fixing mechanism after UV damage?
UV endonuclease after thymine-thymine bonds. Replace with polymerase and ligase. In bacteria, photolyase fix directly.
A patient has fever, HA, malaise, URI and then sudden appearance of erythematous rash on face. Where does this infectious agent replicate?
In bone marrow, think Parvovirus B19. Rash can spread to trunk and extremities.
What is the immune marker for paients with hx of NS, cough, granulomas, and weight loss?
Granulomas, 2ndary TB. CD14!! Monocyte-macrophage cell line.
How do you tell the difference between reactive hyperplasia and malignancy in LN?
Biopsy in LN. If it’s monoclonal - most likely malignant.
What is the difference between follicular, sinus, and diffuse hyperplasia?
Follicular - follicles increase in size and number. Sinus - sinuses enlarge and fill w/ histiocytes. Diffuse - architecture is effaced with LY, and MO. Malignancy - just changes everything.
What is the significance of the Kozak consensus?
It’s a sequence that occurs right upstread from AUG, start codon. If there is a purine 3 bases upstream, key factor in initiation. Mutation in this position has been linked to thalassemia.
What is the mechanism of B12 absorption?
B12 binds with R-protein that keeps t protected from acids till stomach where it attaches onto IF. R protein is then cleaved in duodenum leaving only IF-B12. This complex allows it to pass via SI and get absorbed in distal ileum.
What deficiency do you often give paraenterally?
B12. Because if there’s a malabsorption problem, then giving B12 is going to be useless. (malabsorption=terminal ileal disease, no intrinsic factor, gastric atrophy)
What is the cause of a patient’s splenomegaly who has pyruvate deficiency?
RBCs cannot make glycolysis so any deficiency in glycolysis leads to lysis. Work hypertrophy!! because spleen has to clean it all up.
A person goes to Africa with prophylatic medication and comes back jaundiced with RBCs that stain dark incusions with crystal violet. Inheritance pattern?
G6PD deficiency. It’s X-linked recessive inheritance. Heinz bodies stain that way. When in doubt…structural - AD, enzymatic - AR. Hence hereditary spherocytosis - AD.
Mechanism of MM renal disease?
Amyloid deposits in kidneys (Bence-Jones casts), hypercalcemia -> metastatic calcifications, and inflammation/infiltration by giant cells/plasma cells respectively.
