Want to know Flashcards
(25 cards)
Apoptosis
active process; uses ATP.
USMLE wants you to know hepatocellular death in hepatitis is due to T-cell-mediated
apoptosis.
“apoptosis caused by activation of death receptor extrinsic pathway”;
Menstruation is apoptosis, not atrophy. Menopause is atrophy.
Coagulative necrosis
cellular architecture is maintained.
- Myocardial infarction and acute tubular necrosis are HY examples.
Liquefactive necrosis
cellular architecture not maintained + dissolved by hydrolytic enzymes.
- Refers to 1) abscesses and 2) anything CNS-related.
Caseous necrosis
1) TB; 2) fungal infections; and 3) Bartonella henselae (cat-scratch disease).
Enzymatic-fat
Enzymatic fat necrosis = acute pancreatitis à pancreatic lipases dissolve
surrounding architecture + chelate Ca2+ à saponification (soap formation).
Non enzymatic fat: breast trauma
Fournier gangrene
necrosis of perineum/scrotum in advanced diabetes
Cystic medial necrosis
aortic dissection and aneurysm.
Marfan and Ehlers-Danlos, and systemic hypertension.
“Red neurons”
answer for what will be seen acutely with ischemic infarction of the CNS. This refers
to their strong eosinophilic (pink) staining with H&E.
astrocyte.
responsible for scar formation in CNS,
Cellular swelling
̄diminished Na+/K+ ATPase activity.
reversible
APC
- Mutations cause Familial Adenomatous Polyposis (FAP); chromosome 5; AD.
- 100% cancer risk.
- FAP + soft tissue (e.g., lipoma) or bone tumors (e.g., of the skull) = Gardner syndrome.
- FAP + CNS tumors = Turcot syndrome.
BCL-2
- Overexpressed in follicular lymphoma (most common indolent non-Hodgkin lymphoma) as
a t(14;18) translocation. - Follicular lymphoma will present as waxing/waning painless lateral neck mass over 1-2
years in an adult. - USMLE might give research-type Q where BCL-2 is overexpressed (unrelated to follicular
lymphoma) and they ask what would be expected à answer = increased lifespan of
population of cells (makes sense, since anti-apoptotic molecule).
BCR-ABL
- HY for chronic myelogenous leukemia (CML).
- t(9;22) translocation of these two genes (aka Philadelphia chromosome) codes for a “fusion
protein.” = an oncogenic tyrosine kinase. - CML is answer for leukemia when the Q gives you lots of myelo-sounding cells (i.e.,
myelocytes, promyelocytes, metamyelocytes). 4/5 Qs on USMLE that mention these cells are
CML. Leukocyte ALP will be low.
BRCA1/BRCA2
“recombinational ds-DNA repair.”
c-KIT
mutated in some gastrointestinal stromal tumors (GIST).
c-MYC
- Overexpressed in Burkitt lymphoma (a type of NHL) as a t(8;14) translocation.
- Codes for a transcription factor.
- Burkitt lymphoma will be mass of the jaw or abdomen.
“starry sky” appearance
- The macrophages are referred to as “tingible body” macrophages (correct, not tangible),
where apoptosis occurs.
HER2/neu
(ERBB2)
Tyrosine kinase expressed in some breast cancers.
JAK2
Can be activated in polycythemia vera, essential thrombocytosis, and myelofibrosis.
increased proliferation of hematopoietic stem cells,
EPO is low, not high, in PV.
- Essential thrombocytosis: platelets over a million (NR 150-450,000).
Pain or discoloration in tips of fingers or give hyperviscosity-type
findings. Bone marrow will show increased megakaryocytic proliferation - Myelofibrosis: teardrop-shaped RBCs (dacrocytes) and/or “dry tap” on
bone marrow aspiration.
Massive splenomegaly is seen in basically all questions. NBME can
write the answer as simply “defective hematopoiesis” for myelofibrosis.
KRAS
Proto-oncogene; codes for a GTPase (i.e., always active / cannot shut off).
- First gene mutated in colonic neoplasia.
Usually starts as a
dysplastic polyp prior to progression to overt colon cancer.
- Colon cancer often develops as a result of progressive mutations. In other words, first KRAS, then PTEN, then DCC, then TP53.
- If they tell you a colon cancer has metastasized and force you to choose a gene that’s
mutated, go with TP53 (codes for p53 protein). - If they tell you a polyp is seen and there is no evidence of invasion of the stalk, choose
KRAS. This is on NBME exam. - colon cancer has metastasized : TP53 (codes for p53 protein).
- polyp with no evidence of invasion of the stalk, choose
KRAS.
MSH2/6
MLH1
PMS2
- Hereditary non-polyposis colorectal cancer (HNPCC). (Lynch synd)
- Mismatch repair genes; mutations cause “microsatellite instability.”
Rb
- Congenital retinoblastoma (i.e., leukocoria in 1-year-old) and osteosarcoma.
- (two hits required, AD ).
- RB protein is normally in a complex with E2F, a transcription factor, repressing it and
preventing cell cycle progression.
CDK/Cyclin complexes then phosphorylate RB, releasing it
from E2F.
E2F then goes to the nucleus and transcribes genes à cell cycle progression.
