Hema/Onco 2 Flashcards

1
Q

What is a complication of using fibrinolytic drugs for acute MI?

A

Fibrinolytics can cause reperfusion arrhythmia upon clot lysis and arterial re-opening, although these arrhythmias are usually benign.

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2
Q

Contraindications for using fibrinolytics.

A
Hemorrhagic stroke
Ischemic stroke w/in one year
Active internal bleeding
BP >180/110
Suspected dissecting aneurysm
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3
Q

What condition does dermatomyositis have a strong association with?

A

Dermatomyositis may commonly present as a Paraneoplastic syndrome due to its strong association w/ malignancy (lung, colorectal, NHL, ovarian).

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4
Q

What is the pathogenesis of Peau d’orange and how does it manifest?

A

Cancerous cells obstruct the lymphatic drainage of the breast after spreading to dermal lymphatic spaces. Skin findings appear as an erythematous, itchy breast rash w/ skin texture similar to an orange peel.

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5
Q

What gene mutations are associated w/ hereditary breast cancer? What is the mechanism need for a cancer of this mutation to manifest?

A

BRCA-1, BRCA-2 (tumor suppressor genes).

*Requires a 2-hit LOSS of function for cancer to manifest.

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6
Q

What are Auer rods, what type of stain may be used to identify them, and in what disease may they be found?

A

Auer rods can be found in myeloblasts (neutrophil line) as rod-shaped granules.
They stain with myeloperoxidase (red stain).
Found in abundance in AML M3 (Acute promyelocytic leukemia).

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7
Q

Why are 5HT3 receptor antagonists useful for chemotherapy-induced vomiting?

A

The CTZ has 5HT3 receptors, as well as D2 and NK1 receptors. 5HT3-receptor antagonists (Odansetron) will prevent the chemotherapeutic (emetic) drugs from stimulating the 5HT3 receptors of the CTZ.

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8
Q

If you see an older man or postmenopausal women who presents with microcytic hypochromic anemia, what should you evaluate for?

A

Microcytic hypochromic anemia is commonly due to iron deficiency. If these patients have no obvious reason for being iron deficient, suspect GIT malignancy w/ occult blood loss. Evaluate w/ iron studies and endoscopy.

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9
Q

What type of infectious organisms are sickle cell patients at risk of contracting?

A

All sickle cell patients eventually become asplenic and will no longer be able to fight off encapsulated organisms. The MC would be S. pneumoniae, w/ H. influenzae next. In children, Salmonella is commonly causes osteomyelitis in children.

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10
Q

What are the complications of taking Methotrexate? What is the treatment for its toxicity?

A
MTX tends to target rapidly dividing cells, such as those in the GIT and bone marrow.  As such, it can cause aphthous ulcers and pancytopenia.
Folinic acid (Leucovorin) can reverse these effects if given early, since it doesn't need DHFR to be converted to THF.
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11
Q

What effect do proteasome inhibitors (Bortezomib, boronate-containing dipeptide) have on Multiple Myeloma?

A

In MM, neoplastic B cells mature and produce large amounts of Ig, and proteasomes work to break down damaged proteins so their parts can be re-used. Proteasome inhibitors accumulate toxic intracellular proteins and induce apoptosis of malignant plasma cells.

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12
Q

Why is DIC commonly associated w/ sepsis? What do the lab tests look like?

A

G(-) infections that cause sepsis (ex. secondary to UTI) can expose the blood to procoagulants, ff. by compensatory thrombolysis. This leads to consumption of coagulation factors, coagulopathy, and bleeding.
(Inc. PT, inc. PTT, dec. PC, dec. fibrinogen, inc. fibrin degradation products)

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13
Q

What mutation commonly causes Primary hemochromatosis and what is the pathogenesis?

A

The HFE protein forms a complex w/ transferrin receptor to act as a sensor for iron stores (hepatocytes, enterocytes). Inactivating mutation causes cells to detect falsely low iron levels – enterocytes absorb more iron, less hepcidin released by liver cells and thus inc. ferroportin expression on enterocytes – more iron released into blood, iron overload.

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14
Q

Triad for body iron levels > 20g (Hemachromatosis)

A

Micronodular cirrhosis
Diabetes mellitus
Skin pigmentation (“bronze diabetes”)

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15
Q

Why do you get “dry tap” aspirate in Hairy Cell Leukemia?

A

HCL is an indolent B cell neoplasm caused by infiltration of bone marrow and RES. This can cause fibrosis and BM failure, resulting in pancytopenia and “dry tap” aspirate on bone marrow biopsy.

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16
Q

How do conditions like B-thalassemia affect HbA1c levels (diabetes)?

A

Glucose diffuses freely across RBC membrane, so HbA1c elevation directly correlates w/ average blood glucose. Low and high turnover states can increase or decrease HbA1c levels, respectively – interpret cautiously. For example, B-thalassemia has dec. HbA synthesis, so HbA1c may seem low.

17
Q

Leukemoid rxn vs. Chronic myelogenous leukemia

[labs]

A

> LR: inc. neutrophil ALP (from granules); predominant Metamyelocytes (have granules vs myelocytes); Dohle bodies; assctd. w/ infection, malignancy, hemorrhage).
CML: dec. ALP (low activity of mature granulocytes, abnormal); predominant Myelocytes (no granules); basophilia, eosinophilia; confirm w/ BCR-ABL.

18
Q

What mutation interferes w/ the signal transduction pathway of Polycythemia vera?

A

JAK2 acts as the middle-man b/w EPO receptor and STAT, w/c translocates to nucleus after phosphorylation by JAK2, to induce transcription.
In PV, JAK2 is mutated – constitutive activation of kinase domain – clonal proliferation of myeloid cells.

19
Q

Rb protein is the checkpoint before G1 cells progress to S phase. When is Rb protein active and inactive?

A

> Active - hypophosphorylated: cell stimulated by GFs – activates cyclinD-CDK4 – Rb activated – E2F released to allow progression.
Inactive - hyperphosphorylated: inactive Rb binds to E2F – inhibits transcription.

20
Q

How is skin necrosis a complication of Warfarin therapy?

A

Warfarin inhibits activation of vit k-dependent factors. Since Protein C has shorter half-life than the clotting factors, procoagulation persists, leading to a transient hypercoagulable state. Clot formation interrupts blow flow to skin, causing necrosis.