Heme/Onc 2 Flashcards

1
Q

Cause of infectious mononucleosis (aka mono)

A

EBV

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2
Q

Symptoms of mono

A
Sore throat
Malaise
Lymphadenopathy
Myalgias
Splenomegaly
Fever
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3
Q

What is seen on a peripheral blood smear of someone with mono?

A

Atypical lymphocytes —- activated CD8+ cytotoxic T-lymphs

They destroy virally infected B-lymphs — you see them ‘conforming’ to the border of a neighboring cell

I like to think it looks like they’re eating them OM NOM NOM

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4
Q

Describe the histo characteristics of reticulocytes

A
  • Bluish cytoplasm (basophilic)
  • rRNA precipitates
  • all seen on Wright-Giema stain
  • Slighly larger than mature RBCs

No mitos, nucleus, golgi, histones!

These are released into the bloodstream after tx for iron deficiency anemia (think super fast production so they don’t have time to mature in the BM)

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5
Q

Describe the spleen of a young adult with sickle cell disease

A
  • After repeated splenic infarctions => splenic atrophy and fibrosis
  • Think continual vasoocclusion
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6
Q

What are classic causes of megaloblastic anemia (think macrocytic w/ impaired DNA synthesis)?

A
  • Vit B12 deficiency
  • Folic acid deficiency

Pts w/ sickle cell and other chronic hemolytic anemias are predisposed to these b/c of increased erythrocyte turnover

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7
Q

What is ristocetin?

A

Activates vWF => binds GpIb

Ristocetin aggregation test measures in vitro vWF dependent platelet aggregation

Doesn’t work in vW disease or Bernard-Soulier Syndrome (deficiency GpIb receptors)

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8
Q

p53

A
  • Tumor suppressor gene
  • Controls cell division and apoptosis

Inactivated in many tumors!

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9
Q

Aplastic anemia

A
  • Pancytopenia
  • Low retic count
  • Absent splenomegaly
  • No lymphadenopathy
  • Fat cells and stroma in bone marrow biopsy

Clinical
- Easy bruising

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10
Q

What’s the first thing you want to rule out when a pt comes in w/ findings for iron deficiency anemia?

A

BLOOD LOSSSSSS!

Especially occult loss from GI tract

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11
Q

What are the two most common cerebellar tumors (and brain tumors) in children?

A

1) Pilocytic astrocytomas

2) Medulloblastomas

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12
Q

How do you differentiate between pilocytic astrocytomas and medulloblastomas?

A

Get an MRI:

  • Meds are only solid
  • PAs are solid and cystic (come up white - liquid)

Both in cerebellum

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13
Q

What are the most common cancers in women? Excluding skin cancer

A

1) Breast
2) Lung
3) Colon

Mortality

1) Lung
2) Breast
3) Colon

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14
Q

What is increased in aplastic anemia?

A

Erythropoietin levels

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15
Q

What type of necrosis do you see in TB?

A

Caseous

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16
Q

Caseating granulomas of TB contains which type of immune cell?

A
  • Large epithelioid macros
  • Have pale pink granular cytoplasm
  • Surface marker CD14 at periphery

CD14 is associated w/ all monocyte/macrophage cell lineage

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17
Q

Name the classes of adhesion molecules

A
  • Integrins
  • Cadherins
  • Selectins
  • Ig superfamily
18
Q

How do integrins interact to ECM?

A

Bind collagen, fibronectin, and laminin

19
Q

Argatroban

A
  • Binds directly to thrombin active site
  • Prevents conversion of fibrinogen to fibrin

Used to treat heparin-induced thrombocytopenia

20
Q

Western blotting identifies…

A

Proteins

21
Q

Northern blotting identifies…

A

specific RNA sequences

22
Q

Southern blotting identifies…

A

specific DNA sequences

23
Q

Which 2 substances drive angiogenesis?

A
  • Vascular endothelial growth factor (VEGF)

- Fibroblast growth factor (FGF)

24
Q

Raltegravir

A
  • Integrase inhibitor
  • Disrupts HIV genome integration into host cell’s chromosomes
  • Therefore => it prevents host cellular machinery from being used to synthesize HIV mRNA
25
Q

Pol gene mutations

A
  • Happens due to HIV drug resistance

- These mutations create acquired resistance to HIV reverse transcriptase inhibitors and HIV protease inhibitors

26
Q

What is methemoglobin?

A

Formed when Fe++ (ferrous) in heme is oxidized to Fe+++ (ferric)

Results from drug exposures (dapsone, nitrites), enzyme deficiencies, and hemoglobinopathies

27
Q

Labs of CO poisoning

A
  • Elevated carboxyHb
  • Normal PaO2
  • Normal methemoglobin
28
Q

Life cycle of a B cell

A
  • Precursors proliferate and mature in bone marrow
  • Mature B cells migrate to lymphoid organs/peripheral tissues => exposed to Ags
  • At first exposure => clone activated
  • Some activated clones differentiate into plasma cells that release IgM (T-cell independent)
  • Most activated clones go to lymphoid follicles (in lymph cortex) => creates germinal centers
  • Isotype switching (IgM –> whatever) occurs in germinal centers
29
Q

Describe isotype switching

A
  • Occurs in response to new Ag
  • Occurs in germinal center of lymphoid cortex
  • Required CD40 receptor on B cells w/ CD40 ligand expressed by activated T cells
30
Q

KRAS

A
  • A proto-oncogene
  • Activated in tumor cells
  • Increases cellular response to mitogenic stimuli
31
Q

How do you reverse the effects of heparin?

A

Protamine

  • Binds hep => chemical inactivation
32
Q

How do you reverse the effects of warfarin?

A
  • Vit K

- Fresh frozen plasma

33
Q

Paroxysmal nocturnal hemoglobinuria

A

TRIAD:

1) Hemolytic anemia
2) Hypercoagulability
3) Pancytopenia

  • Acquired mutation in PIGA gene
  • Deficiency in CD55 and CD59 complement inhibitor proteins
34
Q

What is the fastest way to reverse Warfarin’s effects?

A

Fresh frozen plasma

Vit K facilitates clotting factor re-synthesis (takes time)

35
Q

Why does a bruise turn green after several days?

A
  • Heme is converted to biliverdin (verde) via heme oxygenase

- It’s then converted to unconjugated bilirubin via biliverdin reductase

36
Q

How do you initiate hemolytic anemia in someone deficient in G6PD?

A
  • Give them anti-malarial drugs! (they’re going to Africa usually)

Labs:

  • Anemia
  • Reticulocytosis
  • Indirect hyperbilirubinemia
  • Smear w/ Heinz bodies

X-linked recessive

37
Q

What are Heinz bodies?

A

RBCs w/ dark, intracellular inclusions that stain w/ crystal violet

38
Q

Isoniazid effects on heme production

A
  • Inhibits pyridoxine phosphokinase => Vit B6 deficiency => deficiency in ∂-aminolevulinate synthase (RLS of heme synthesis)

Causes:

  • Decrease Hb/HCT
  • Decreased MCV
  • Sideroblastic anemia
39
Q

A “retained dead fetus” can cause what?

A

DIC and progressive hypofibrinogenemic

Must monitor fibrinogen and platelets to identify onset of DIC

40
Q

Findings in DIC

A
  • Prolonged PTT and PT
  • Thrombocytopenia
  • Microangiopathic hemolytic anemia
  • Low fibrinogen
  • Elevated D-dimers
  • Low Factor 5 & 8 levels
41
Q

Warfarin-induced skin necrosis

A
  • Warfarin inhibits protein C/S => can cause necrosis
  • Especially in people deficient in protein C/S
  • Usually seen in first few days of admin