Bootcamp Incorrects Flashcards

1
Q

S: Hematology & Oncology: Pathology
Q: Which vitamin causes megaloblastic anemia with elevated levels of homocysteine and normal levels of methylmalonic acid?

A

Folate (B9)

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2
Q

S: Hematology & Oncology: Pathology
Q: Older pt presents with hypercalcemia, anemia, elevated BUN, and RBC rouleaux formation on PBS is suggestive of?

A

Multiple Myeloma, a plasma cell malignancy.

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3
Q

S: Hematology & Oncology Pharmacology
Q: When and how do proteasome inhibitors work?

A
  • Induce cell cycle arrest at the G2-M phase, leading to apoptosis.
  • Carfilzomib, Bortezomib, and ixazomib inhibit the degradation of ubiquitinated proapoptotic proteins, leading to their accumulation and eventual cell death.
  • Often used in Multiple Myeloma and mantle cell lymphoma due to the vast increase in cell division.
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4
Q

S: Hematology & Oncology: Pharmacology
Q: What are some common side effects of proteasome inhibitors?

A

Peripheral neuropathy, hepatotoxicity, thrombocytopenia, neutropenia, and an increased risk of herpes zoster reactivation.

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5
Q

S: Immunology: Pathology
Q: Describe IgA vasculitis:

A

aka Henoch-Schönlein purpura (HSP).
- Hematuria (dark urine) + Palpable purpura
- Triad of arthralgia, abdominal pain (increased risk of intussusception), and palpable purpura on the buttocks and legs.
- Typically occurs in children 3 to 11 years old shortly after an URI
- IgA and C3 mediated small vessel leukocytoclastic vasculitis
- Light microscopy will show mesangial proliferation
- Immunoflurescence will reveal IgA-based immune complex deposition in the mesangium.
- usually self limited but can be complicated by glomerulonephritis (IgA nephaopathy) and end-stage renal disease
- IgA vasculitis can cause nephritic syndrome, decreased GFR leading to oliguria, azotemia, and hypertension. Pts to be observed, severe cases give corticosteroids.

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6
Q

S: Immunology
Q: Describe SCID (Severe combined immunodeficiency):

A
  • Presents in early childhood with failure to thrive, chronic diarrhea, serious viral, bacterial, and fungal infections, and oral thrush
  • defect in the IL-2R-gamma chain and inherited through an XLR pattern
  • diagnosed by an absent germinal center on lymph node bx, absent T cells on flow cytometry, and absent thymus shadow on CXR
  • Candida albicans antigen skin test is a historical test
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7
Q

S: Hematology & Oncology: Pharmacology
Q: In chronic opioid users, which side effects are considered minimally tolerated?

A

Constipation or miosis

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8
Q

S: Immunology: Pathophysiology
Q: What process is most likely defected in Ataxia telangiectasia?

A

Non-homologous end- joining

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9
Q

S: Hematology & Oncology: Pathophysiology
Q: What are the adverse side effects of Bleomycin?

A

Pulmonary fibrosis, leading to a restrictive pattern on PFTs. RLDs are characterized by decreased lung volumes with a normal or elevated FEV1/FVC ratio.

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10
Q

S: Hematology & Oncology: Pharmacology
Q: How does Dexrazoxane work? (a cytarabine)

A

Coadministered with Anthracyclines (Daunorubicin, doxorubicin; binds with topoisomerase II to cleave DNA in cancer cells)
- Function to prevent cardiotoxicity. Works by chelating and sequestering iron, thereby minimizing free radical reactions within cardiomyocytes.

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11
Q

S: Immunology: Pathophysiology
Q: What is accumulated in SCID caused by ADA (adenosine deaminase) deficiency?

A

Deoxyadenosine and dATP

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12
Q

S: Immunology: Pharmacology
Q: What are some examples of live-attenuated vaccines?

A

Influenza (intranasal), MMR, varicella, smallpox, rotavirus, polio

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13
Q

S: Immunology: Pharmacology
Q: What is the composition of live-attenuated vaccines?

A

Weakened, live viral particle

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14
Q

S: Immunology: Pharmacology
Q: What kind of immune response occurs with live-attenuated vaccines?

A

Cellular humoral

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15
Q

S: Immunology: Pharmacology
Q: What is the immune duration for live-attenuated vaccines?

A

Long, often lifelong

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16
Q

S: Immunology: Pharmacology
Q: What is the effectiveness of live-attenuated vaccines?

A

Greater than inactivated

17
Q

S: Immunology: Pharmacology
Q: What is safety regarding live-attenuated vaccines?

A

Contraindicated in high-risk patients (eg, pregnancy, immunodeficiency)

18
Q

S: Immunology: Pharmacology
Q: What is the relative stability of live attenuated vaccines at room temperature?

A

Low

19
Q

S: Immunology: Pharmacology
Q: What are some examples of inactivated vaccines?

A

Influenza (intramuscular), hepatitis A, rabies, polio

20
Q

S: Immunology: Pharmacology
Q: What is the composition of inactivated vaccines?

A

Inactive viral particle or antigen

21
Q

S: Immunology: Pharmacology
Q: What kind of immune response occurs with inactivated vaccines?

A

Humoral

22
Q

S: Immunology: Pharmacology
Q: What is the immune duration for inactivated vaccines?

A

Shorter, usually requires a booster

23
Q

S: Immunology: Pharmacology
Q: What is the effectiveness of inactivated vaccines?

A

Lower

24
Q

S: Immunology: Pharmacology
Q: What is safety regarding inactivated vaccines?

A

Safe

25
Q

S: Immunology: Pharmacology
Q: What is the relative stability of live attenuated vaccines at room temperature?

A

High

26
Q

S: Hematology & Oncology: Pathology
Q: What labs would you expect in a patient with von Willebrand Disease?

A
  • Normal plate count with an elevated bleeding time
  • normal prothrombin time (PT)
  • elevated partial thromboplastin time (PTT)- impaired factor VIII function
  • normal fibrinogen values
  • normal peripheral blood smear
  • abnormal ristocetin cofactor assay
27
Q

S: Hematology & Oncology: Pathology
Q: Abnormal platelet aggregation in a ristocetin cofactor assay is suggestive of what?

A

Defective or deficient vWF or deficient platelet GPIb receptors (seen in Bernard-Soulier syndrome)

28
Q

S: Immunology: Pharmacology
Q: Which medications aim to minimize the PD-L1 (on cancer cells) and PD-1 interaction in cases of melanoma?

A
  • Pembrolizumab is a PD-1 receptor inhibitor
  • Atezolizumab is a PD-L1 inhibitor
29
Q

S: Hematology & Oncology: Pharmacology
Q: What can you administer to increase the release of vWF from the Weibel-Palade bodies of endothelial cells to improve platelet aggregation?

A

Desmopressin (DDAVP)

30
Q

S: Immunology: Pathophysiology
Q: Pt presents with swelling of the lips and PMH of recurrent swelling of the lips, face, larynx, and GIT. What’s the diagnosis, why is it occurring?

A

C1 esterase inhibitor deficiency resulting in unregulated kallikrein activity, leading to increased bradykinin synthesis.

31
Q

S: Hematology & Oncology: Pathophysiology
Q: What is the relationship between Placental abruption and DIC?

A

PA is the mc cause of DIC in pregnancy. PA can lead to the release of tissue factor (thromboplastin) into the maternal circulation, causing widespread activation of the clotting cascade, fibrin deposition, and fibrinolysis.

32
Q
A