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Heme/Onc Flashcards

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1
Q

A patient with a family hx of breast cancer most likely has a gene defected in what?

A

BRCA. increased risk of breast and ovarian cancer. plays role in gene repair and transcription

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2
Q

What is a good sensitive marker for bladder cancer in their malignant potential?

A

Involvement of muscular layer. Painless hematuria is bladder cancer.

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3
Q

increased activity is most likely responsible for conversion of pro-carcinogens to carcinogens

A

P450 microsomal monooxygenase. Metabolizes steroids, EtOH, toxins, and other foreign substances but can also convert pro-carcinogens to carcinogens.

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4
Q

What are the patches in mycosis fungoides called?

A

Proliferating CD4+ infiltrates skin. Cuse pautrier microabscesses.

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5
Q

What chromosome is affected in the disease that has a waxing and waning lymphadenopathy?

A

Follicular lymphoma - t(14;18)

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6
Q

In megaloblastic anemia, why should you give folate and B12 concurrently?

A

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.

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7
Q

How does ondansetron work?

A

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.

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8
Q

Where are 5HT3 receptor located?

A

In presynaptic nerve terminals of vagus nerve in GI tract and centrally in the chemoreceptor trigger zone and solitary nucleus/tract

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9
Q

First thing to look at with microcytic anemia?

A

GI bleed –> iron deficiency anemia

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10
Q

Why do people who have recently started warfarin can develop a rash/necrosis?

A

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

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11
Q

what form of cancer has risen dramatically in the last few decades for women

A

lung, both in mortality and incidence

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12
Q

If P(50) for hemoglobin went from 26mmHg to 20mmHg, what would happen?

A

Polycythemia - you have increased affinity for oxygen. Less oxygen at tissue level, tissue hypoxia and a result, reflex polycythemia.

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13
Q

An African American women with photodistributed skin rash and arthralgia with proteinuria has pancytopenia. Explain.

A

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.

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14
Q

What bone pathology are sickle cell patients at risk for?

A

Osteomyelitis. Likely salmonella, followed by Staph aureus and E coli

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15
Q

Are sis/TGF-alpha/ERB-B1 onco or tumor suppressor genes? If so, what do they code for?

A

sis - astrocytoma/osteo. ERB-B1: Lung SCC. TGFalpha-astro, HCC.

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16
Q

Pt has many immature cells (band forms, metamyelocytes, myelocytes) and few bands. leukcoyte alkaline phosphatase is low. Diagnosis?

A

CML. Leukemoid rx has normal/elevated in leukemoid rx.

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17
Q

Patient has thrombocytopenia with an ezcematous skin rash and recurrent URI. What infx is he at risk for?

A

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.

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18
Q

Platelet derived growth factor are found in what type of leukemia?

A

CML

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19
Q

A patient w/ hx of heavy periods and nosebleeds has a Hgb of 9.2 and MCV of 72, ferritin is low. Why?

A

Pt has vWF deficiency. also may have gingival/mucosal bleeding. Bleeding results in iron deficiency anemia

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20
Q

In hereditary spherocytosis, why is MCHC elevated?

A

Mild dehydration of RBC

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21
Q

If a person is vit B12 deficient, how do you differentiate b/w the causes?

A

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).

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22
Q

Monoclonal abx against CD21 is helpful for treating what virus?

A

EBV gp350 binds with CD21 normally on surface of B cells and nasopharyngeal epithelial cells.

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23
Q

When does HbA2 switch to HbA

A

During the first 6 months of life. First few weeks is all HbF, startnig at 10-12 wks of gestation.

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24
Q

What is the role of 2,3 DPG and ho does it relate to fetal hemoglobin?

A

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

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25
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.
26
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.
27
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.
28
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.
29
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.
30
What is the immune marker for paients with hx of NS, cough, granulomas, and weight loss?
Granulomas, 2ndary TB. CD14!! Monocyte-macrophage cell line.
31
How do you tell the difference between reactive hyperplasia and malignancy in LN?
Biopsy in LN. If it's monoclonal - most likely malignant.
32
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.
33
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.
34
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.
35
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)
36
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.
37
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.
38
Mechanism of MM renal disease?
Amyloid deposits in kidneys (Bence-Jones casts), hypercalcemia -> metastatic calcifications, and inflammation/infiltration by giant cells/plasma cells respectively.
39
What is CO poisoning on PaO2, methemo, and carboxyhemo?
PaO2 is unchanged. Carboxy goes up. Met nope, nothing. Dissociation curve plateaus out with left shift.
40
Guy takes nitrites. How will that affect the oxygen in his blood?
Won't change PaO2. Will change everything else as methemoglobin cannot bind oxygen, instead to cyanide. Causes dusky discoloration to skin.
41
Common things that cause sub and supra therapetutic INRs?
sub: rifampicin, phenobarb, phenytoin. supra: cimetidine, amiodarone, bactrim inhibit warfarin metabolism
42
Are there any symptoms of sickle trait?
Sometimes hematuria and inability to concentrate urine. Note: sodium metabilsulfate will cause sickling - sickling test.
43
Mom is A neg, baby is B neg. Why no problem?
HDN and erythroblastosis fatalis are only in O type moms as IgG can cross but IgM cannot. IgM are seen in anti-A and anti-B in A / B blood patients
44
Why would RBCs sometimes use a pathway that makes no energy as opposed to some?
From 1,3 biphosphoglycerate to 3-phosphoglycerate, it produces one ATP. Problem is...2,3-biphosphoglycerate allows for oxygen release as it decreases affinity for heme with oxygen. So in hypoxia, chronic anemic states, RBC chose this route instead.
45
Why is the only vitamin that can last for several years, why?
Vit K, colonic bacteria make that shit.
46
What are lab values of hemolysis?
Decreased haptoglobin (binds free hemoglobin released in hemolysis), increased LDH, hemoglobin, and bilirubin
47
What is the inheritance pattern of Li-Fraumeni syndrome?
AD. p53 gene. THese people have cancers everywhere at young ages and run in families. p53 stops cells at G1/S phase for repair.
48
What would you see in a patient with single stranded, non-enveloped DNA virus?
Parvovirus - erythema infectiosum. Fifth disease. Aplastic crisis + hydrops fetalis.
49
What is the mechanism of what vit K does?
Cofactor for hepatic microsomal carboxylase that converts glutamyl residues into y-carboxyglutamates. Need for VII, IX, and X.
50
What is the mechanism of leucovorin rescue?
It makes THF without needing DHF (vit B9, product after folic acid pass in liver) and DHF reductase
51
What are the findings of a mom who has DIC after baby died?
progress hypofibringonemia. Monitor elevated fibrin split products (D-dimer), MAHA, thrombocytopenia, PTT/PT increase, low V and VIII/fibrinogen
52
What is teh difference in mechanism b/w low and high dose aspirin
Low - COX1, high - COX 1/2. On both platelets and vascular endothelial cells that proces PGH2. Reduce TXA2 and impair PGE2/PGI2. PPI can help reduce risk of GI bleed.
53
What is salicylism and Samter's triad?
Salicylism: vertigo, tinnitus, hearing loss with high dose ASA. Samter's triad: asthma, nasal polyposis, and aspirin hypersensitivity (nasal sx's, bronchospasm, flushing).
54
Do methylmalonic acid levels rise or decrease in atrophic gastris?
Increase. Along with gastrin, decrease in B12, intrinsic factor production, no acid.
55
How do you differentiate b/w B cell ALL and T cell ALL?
B cells, CD 10, 19, 20. T cells CD<#10. T cells also have anterior mediastinal mass that can lead to SVC syndrome (dysphagia, dyspnea, stridor)
56
What is the mitotic and histology of Burkitt's?
High mitotic index. Histology: uniform, round, diffuse LY. associated with c-myc.
57
The product used for treatment of DI is what and has what effect in terms of bleeding?
Desmpopressin releases factor VII and vWF. Treat hemophilia A, not B. ADH analog. Endothelial cells to release former factors.
58
What are some symptoms of polycythemia vera?
1) Blurry vision, HA. 2) Itching after bathing (mast cell release), 3) plethora: flushed face 4) Venous thrombosis - Budd chiari
59
A patient on chemo develops frequent urination, suprapubic pain, hematuria, dysuria, etc. What is the metabolite responsible?
Acrolein from cyclophosphamide use. Treat with mesna.
60
What screening test are you going to use to check for the virus that can make mature B cells proliferate nonstop?
Monospot for EBC immortalization
61
What cell is responsible for iron absorption? What is the mechanism?
Hepcidin in the liver. Fe3+ is absorbed via DMT-1. Can go into ferritin and stored/excreted via stool in entereocyte or enter circulation via ferroportin-1 and transported by transferrin, entering cells. Hepcidin downgrades ferroportin-1. So in low levels of iron, low levels of hepcidin.
62
How would you describe the histology of a patient with sore throat, malaise, LAD, myalgia, and fever.
Hugging of CD 8+ T cells to CD21 B-cell infected with EBV
63
How does a spleen look like after multiple ACS in sicklers? (precipitated by URI)
fibrotic, shrunken, brown discolored (hemosiderosis)
64
What symptoms are seen in primary myelofibrosis?
Bone marrow fibrosis with hepatomegalo and splenomegaly (early satiety/abd discomfort) from extramedulallry hemato
65
What is the mechanism for which protons release from O2 in tissues?
In tissues, more CO2 and hence decrease pH. There are ionizable histidine side chains at the N-terminal alpha amino agroup of alpha and beta HgB subunits that bind protons with high affinity when HgB is dexoygenated. Stabilizes deoxygenated form.
66
Sickle cell has macrocytic anemia, why?
More prone to folic acid deficiency because of increased erythrocyte turnover.
67
What is the fusion gene implicated in leukemia that response to vitamin derivatives?
PML/RARalpha
68
What other drug can you give sicklers besides hydroxyurea?
Gardos channel blockers - hinder efflux of K and water from cell, preventing dehydration and sickling. Ca dependent.
69
do steroids increase or decrease hematocrit?
increase because of increased androgens.
70
What are some iron deficient specific syndromes?
Dysphagia (Plummer-vinson syndrome) or koilocnchia, disfigured nails.
71
What is one cell surface glycoprotein cancer cells can use to resist anticancer drugs?
MDR1 gene. ADP dependent transporter that normally pumps out bad stuff in gut /kidneys or brain.
72
What is the relation between population curves and degree of overlap and sensitivity/specificity?
More overlap = decrease of both. Sensitivity/specificity is best when no overlap.
73
What are some precipitating cause of G6PD?
Infx, drugs (antimalarial, bactrim or sulfa drugs, dapsone), fava beans, DKA
74
How do you differentiate b/w DIC and TTP/HUS
DIC has bleeding, prolonged PT/PTT, and low fibrinogen/D-dimer, activation of coagulation cascade
75
How do you differentiate b/w DIC and TTP/HUS
DIC has bleeding, prolonged PT/PTT, and low fibrinogen/D-dimer, activation of coagulation cascade
76
How does the myoglobin oxygen curve lok like?
Hyperbolic to the left. Individual subunits, only has one heme molecule. IN skeletal/cardiac muscle.
77
How does the myoglobin oxygen curve lok like?
Hyperbolic to the left. Individual subunits, only has one heme molecule. IN skeletal/cardiac muscle.
78
How do reticulocytes look on histology, what stain do you use?
Wright-Giemsa stain. Bluish cuz of residual ribosomal RNA
79
What is the most effective anticoagulant against thrombin?
unfractionated heparin. Both LMWH and UHep activated AT III against factor Xa. Only UH can bind both antithrombin and thrombin to allow AT III inactive thrombin
80
What does follicular lymphoma look like under the microscope?
Mostly packed follicles that obscure normal LN architecture.
81
Mom is Rh -. First child is Rh+. Treatment?
None. But she wil need anti-Rh(D) Ig for next baby if Rh+. Type 2 hypersensitivity response.
82
Normal PT/PTT and platelet count with elevated bleeding time? Diagnoses (2 of them)
vWF (may be elevated PTT) or uremia-induced bleeding. Note: Heparin increases PTT.
83
What GI issue results from any type of hemolytic anemia?
Pigmented galstones.
84
Person with OSA has what characteristic in hemoglobin?
Increased hematocrit. Renal cortical cells sense hypoxia and release EPO, 2ndary PV.
85
Person with hemolytic anemia, hypercoagulable state, and decreased blood counts have what molecular problem?
PNH - complement mediated. They don't have GPI which binds CD55 and CD59 which turn off complement. People commonly develop thrombosis lke Budd-Chiari.
86
Circulating erythrocytes cannot make heme because?
They have no mitochondria. Mitochondria needed for heme synthesis. They lose mitochondria when they break off too many times.
87
What do you think about in a patient with anemia with decreased retic, RBC but normaly myeloid and megakarocytic elements?
Pure red cell aplasia. Associated with thymoma and parvovirus. auto abx or CD8 against T lymphocytes.
88
Can HCC and cerebellar hemangioblastomas secrete EPO?
Yes. but rare.
89
What does iron overload look like?
Skeletal deformalities with "mongloid face"
90
What is hemosiderin and what does it look like?
Aggregation of ferritin micelles, basically deposited iron in tissues. have golden yellow brown pigment.
91
How does therapeutic radiation work?
Causes DNA double strand breakage and formation of free radicals via water
91
How does therapeutic radiation work?
Causes DNA double strand breakage and formation of free radicals via water
92
What chemo drug do you give for hairy cell leukemia and why?
Cladiribine. Purine analog that resists degradation by adenosine daminase. Can reach high intracellular concentration and causes dNA strand breaks. Penetrates CNS well.
92
What chemo drug do you give for hairy cell leukemia and why?
Cladiribine. Purine analog that resists degradation by adenosine daminase. Can reach high intracellular concentration and causes dNA strand breaks. Penetrates CNS well.
93
If you have a defect in organic anion transporter, what would be the result or person with hemolysis?
bili is excreted into biliary system by MRP2. Inhibition of this results in it secreting into urine instead as it's conjugated meaning it's water-soluble.
93
If you have a defect in organic anion transporter, what would be the result or person with hemolysis?
bili is excreted into biliary system by MRP2. Inhibition of this results in it secreting into urine instead as it's conjugated meaning it's water-soluble.

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