General (Malaria, HLA, Cancer) Flashcards

1
Q

Capecitabine

A

converted to 5-FLUOROURACIL in cancer cells

decrease the biosynthesis of pyrimidine nucleotides by inhibiting thymidylate synthase, the enzyme that catalyzes the rate limiting step in DNA synthesis. This results in the “thymineless death” of rapidly growing cells.

LEUCOVORIN increases binding of 5-FU to thymidylate synthase thereby increasing 5-FU t1/2

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2
Q

HLA-B27

A
(MHC class I) individuals are 90x more likely to develop ankylosing spondylitis (destruction of the vertebral cartilage).
•	Also linked to psoriasis, inflammatory bowel disease, and Reiter’s syndrome
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3
Q

HLA-DR2

A

(MHC II) individuals are 130x more likely to develop narcolepsy.
• Also linked to multiple sclerosis, hay fever, and SLE.

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4
Q

HLA-A3/B14

A

MHC I
individuals are 90x more likely to develop hemochromatosis (too much iron adsorption which can lead to internal organ damage).

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5
Q

HLA-DQ2/GQ8

A

MHC II

linked to Celiac disease.

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6
Q

HLA-DR3

A

MHC II

linked to diabetes mellitus type I, Grave’s disease

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7
Q

HLA-DR4

A

MHC II

linked to rheumatoid arthritis and diabetes mellitus type 1

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8
Q

What is the gold standard for diagnosis of Malaria?

A

blood smear

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9
Q

Resistance readily occurs in what two types of malaria?

A

vivax and falciparum

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10
Q

suppressive prophylaxis of malaria uses what drug(s)?

A

chloroquine

alternate = atovaquone/proguanil

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11
Q

Supportive prophylaxis of chloroquine resistant malaria uses what drug(s)?

A

atovaquone/proguanil

alternate = doxycycline

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12
Q

Drugs to treat an acute attack of nonresistant malaria…

A

chloroquine phosphate (oral)

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13
Q

Drug to treat chloroquine resistant P. falciparum or P. vivax?

A

quinine + doxycycline

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14
Q

A child patient arrives in the ED with a severe onset of Plasmodium (malaria) like symptoms. You don’t have time to do a work up to determine the exact species. What is the most likely species? Parenteral Tx?

A

P. falciparum

IV quinidine + doxycyline

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15
Q

chloroquine

A

parasitized RBCs concentrate chloroqine at least 25x

binds ferriprotoporphyrin IX inside vacuole and prevents conversion to hemozoin via heme polymerase.

large doses for prolonged periods cause severe eye damage

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16
Q

Quinine

A

chloroqine resistant P. falciparum

MOA same as chloroquine

cinchonism – permanent vision damage, balance, hearing problems

17
Q

Quinidine

A

IV for severe malaria (parenteral)

blocks Na and K currents (antiarrhythmic)

Tox; cardiac problems

18
Q

Mefloquine

A

Indicated only for the prophylaxis of chloroquine resistant P. falciparum

MOA same as chloroquine

neuropsychiatric reactions (wild dreams +)

19
Q

Atovaquone + Proguanil

A

slow onset
replacing mefloquine for prophylaxis

Atovaquone – depolarizes parasitic mito inhibiting ETC

Proguanil – inhibits DHFR (*increased affinity for malarial DHFR)

GI disturbances

20
Q

Artemisinins and Combinations

A

MOA: heme iron in malarial pigment acts on the drug to produce free radicals

rapid onset
replaces quinidine for severe disease

21
Q

Primiquine

A

drug of choice to eliminate hepatic forms (hypnozoite) of P. vivax/ovale

generates ROS (possibly interfering with ETC)

Tox: hemolytic anemia in G6PD deficiency… antimalarials are bad in people with G6PD def.

22
Q

AML with genetic abnormalities…

t(8, 21)

A
AML M2 (neutrophilic series)-- good prognosis
(myeloblasts over 20%, but not high)
23
Q

AML with genetic abnormalities…

inv(16)

A

AML M4 (monocytic series)– good prognosis

Look for BOTH increased myeloblasts and moncytic cells

24
Q

AML with genetic abnormalities…

t(15, 17)

A

AML M3 (neutrophilic series) – good prognosis

high [promyelocytes] and faggot cells (lots of auer rods)

this type of translocation occurs in all cases!

25
Q

AML with genetic abnormalities…

11q23

A

usually monocytic (M4 or M5) – bad prognosis

26
Q

AML with FLT-3 mutation

A

FLT-3 = tyrosine kinase mutation

⅓ of AML cases

27
Q

AML with multilineage dysplasia

A

All three lines (RBCs, mon, granulocytes) dysfunctional

severe pancytopenia

28
Q

AML, therapy related

A
previous chemo
alkylating agents -- Busulfan
TOPO II inhibitor (Etopaside) 
sometimes (11q23)
very hard to treat
29
Q

4 general things you must know about Acute Lymphoblastic Leukemia

A
  1. malignant proliferation of lymphoid blasts in blood/bone marrow (begins in lymph node!)
  2. classified by immunophenotype (B vs. T)
  3. more common in children
  4. prognosis good
30
Q

T-lymphoblastic leukemia/lymphoma (MUST KNOW)

A

teenage male with mediastinal mass
WBC usually v. high
bad prognosis

31
Q

B-lymphoblastic leukemia/lymphoma

A

several subtypes
TdT+
Rarely Ph+ (philidelphia chromosome positive (this is usually in CML t(9,22))