Q#3 Flashcards

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1
Q

What chromosome translocation is involved in Acute Promyelocytic Leukemia?

A

15 and 17 and 22 and 21.

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2
Q

What are signs of Acute Promyelocytic Leukemia?

A

-Pancytopenia
-DIC, causing bleeding

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3
Q

What is the pathogenesis of Acute Promyelocytic Leukemia (APML)?

How do we treat APML?

A

The translocation between 15 and 17 leads to disruption of the retinoic acid alpha receptors subunits, ultimately causing the decreased production of retinoic acid, a substance used to help myelocytic cells mature. As a result, myeloblasts proliferate excessively and crowd out the bone marrow, leading to pancytopenia.

Treat APML by giving all-trans retinoic acid.

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4
Q

What are Auer rods?

Why are they important?

What condition are they mostly seen in?

A

Auer rods are byproducts that come from myeloblasts.

They help us to differentiate between Myeloid vs Lymphoid Leukemias.

Auer rods are mostly seen in Acute Myeloid Leukemia.

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5
Q

What is a condition associated with Acute Myelocytic Leukemia (AML)?

A

DIC

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6
Q

What are the chromosomal translocations in Acute Lymphocytic Leukemia (ALL)?

A

12 and 21 (children)
9 and 22 (adults)

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7
Q

What is the chromosomal translocation in CML?

A

9 and 22.

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8
Q

What are the two types of ALL?

A

-B cell ALL - in children or adults (85% of all ALL), depending on the translocations.
-T cell ALL - in teenagers (infiltration of the thymus).

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9
Q

How do patients typically find out that they have Chronic Myelogenous Leukemia (CML)?

A

CML patients are usually aysmptomatic and find out incidentally through routine lab work.

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10
Q

What are symptomatic signs of CML?

What do we see on the bloodwork for CML?

A

Fatigue, weight loss, bleeding, early satiety/splenomegaly, Left upper quadrant pain and mass.

Increased overall WBC, with increased number of Neutrophils and Basophils. Decreased Leucocyte Alkaline Phosphatase (low activity in mature leukocytes).

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11
Q

What is a major complication of CML?

How do we treat CML?

A

CML can convert into ALL and AML.

Tyrosine Kinase Inhibitors.

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12
Q

What is the pathogenesis of CML?

A

The translocation of chromosomes 9 and 22, causing the production of the Philadelphia chromosome, causing production of unrelenting tyrosine kinase.

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13
Q

What is they typical age for CML?

A

50-60 years of age.

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14
Q

What is the main difference between Steven Johnson Syndrome (SJS) and Toxic Epidermal Necrosis (TEN)?

A

The amount of surface area involved - SJS is under 10%; TEN is over 30% SA involved.

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15
Q

How do SJS and TEN present?

A

They present with desquamative/blistering lesions on the skin and mucosa. The patients also become febrile. The patients almost always have mucosal involvement. Half of patients have ocular involvement.

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16
Q

What are the main triggers for SJS and TEN?

A

Medications&raquo_space; Infections.

NSAIDs, (Penicillins, Sulfonamides - anti bx), (Carbamazepine, Lamotrigine, Phenytoin - seizure meds).

17
Q

What is the progression of TEN and SJS?

A

They start off with lesions that are flat and red that turn into taut, bullous lesions that tear off when you rub the skin (+Nikolsky sign). It is super painful.

18
Q

How does Erythema Multiforme present?

A

Patients get these classic targetoid-looking lesions on their skin that spread.

19
Q

Is erythema multiforme (EM) the same as SJS and TEN?

A

No, EM is less severe (no Nikolsky sign).

20
Q

What are the two types of EM? What separates them?

A

EM minor - no systemic syx and no mucosal involvement.

EM major - presence of systemic syx and mucosal involvement.

21
Q

What are the main triggers for (Erythema Multiforme) EM?

A

-Infection&raquo_space; Drugs (NSAIDs, Sulfonamides, etc.)

-HSV infection
-Pneumonia

22
Q

What is Ranson’s criteria?

A

A list of clinical findings on admission and after two days that tell us how likely a patient with pancreatitis is to die.

23
Q
A