NBME Pathology Path Block 1 Latest Update
2024-2025 175 Questions and 100% Verified
Correct Answers Actual Exam Guaranteed A+
(Pseudo) Membranous - CORRECT ANSWER: Exhibits membrane composed of fibrin;
necrotic epithelium; and inflammatory cells
Acute Inflammation - CORRECT ANSWER: Rubor (redness); Calor (heat); Tumor
(swelling); Dolor Rapid delivery to site of injury; More neutrophils, less mononuclear
cells
Increase vascular permeability and vasodilation due to retraction of endothelial cells,
endothelial injury, leukocyte-mediated vascular injury, increased transcytosis
Lewis Triple Response: Red Line and Flare (vasodilation), Wheal (vascular leakage)
Arterioles involved first
Acute phase reactions due to IL-1 and TNF: increase sleep, decrease appetite, increase
acute-phase proteins, hemodynamic effects (shock), neutrophilia (pain); Functio laesa
(loss of function)
Angiogenesis - CORRECT ANSWER: Proteolytic degradation of BM; migration of
endothelial cells; proliferation of endothelial cells; maturation Controlled at DLL4/notch
and VEGF
Anthracosis - CORRECT ANSWER: Dark pigments distribute along lymphatics
Aplasia - CORRECT ANSWER: Failure of development of primordium
Apoptosis - CORRECT ANSWER: Oncosis w/ no inflammation (pathologic or
physiologic)
Intact cell membrane
No leakage
Activation of proteases/ endonucleases
Intrinsic: withdrawal of growth factors/ hormones
Extrinsic: Receptor-ligand interaction (FAS and TNF receptor)
Anti-apoptotic= Bcl-2
Ataxia-Telangiectasia mutated (ATM) - CORRECT ANSWER: Activated by mechanisms
that sense dsDNA breaks arrest cell cycle by acting through p53 in G1/S checkpoint and
G2/M checkpoint, inactivation of CDC25 phosphatase disrupts cyclinB-CDK1
Part of network including BRCA-1/BRCA-2: cell damage cycle arrest and apoptosis
ATM and CHEK2 phosphorylate BRCA-1 migrate to DNA colocalization with Fanconi
protein D2 (triggered by Fanconi's anemia protein complex)
BRCA2 carries RAD51 to same site BRCA1, BRCA2 & RAD51 repaire DNA breaks
Atresia - CORRECT ANSWER: Absence of an opening
Atrophy - CORRECT ANSWER: Decrease in size, cell # Physiologic or pathologic Often
reversibleMechanism: decrease metabolic activity decrease protein synthesisIf caused
by decrease blood flow apoptosis Brown Atrophy: due to accumulations of lipofuscin
Autophagy - CORRECT ANSWER: Self/ auto digestion
, Benign Tumor - CORRECT ANSWER: NOT malignant, Small (2-5x normal), well
demarcated (symmetric, distinct margins), slow growing, noninvasive, nonmetastatic,
well-differentiated
Only pushes margins
Age of onset= young
Burkitt Lymphoma - CORRECT ANSWER: (8; 14) translocation alteration of c-myc
increased myc protein
Numerous, pale-body macrophages= "starry sky" appearance
High mitotic index, multiple small nuclei, lack of significant variation in nuclei shape and
size monotonous appearance
Cancer Cachexia - CORRECT ANSWER: Progressive loss of body fat and lean body
mass accompanied by decreased appetite, weakness and lethargy (Malignancies of
Pancreas or colon)
↑ BMR and Hi caloric expenditure remaine,
Cancerogenesis - CORRECT ANSWER: -Cells susceptible to 1. Genetic alteration and
2. Development of progeny that propagate the altered genetic material
-Rapidly turning-over cell populations: Bone marrow hematopoietic precursors, basal
layer keratinocytes, basal layer of glandular or ductal epithelium continually in G1 phase
account for a majority of malignancies
-G0 non-proliferating cells (CNS neurons and cardiac myocytes) don't become
malignant
-Environmental agents or spontaneous mutations cause genetic damage of:
Activation of protooncogenes (Myc, Cyclin D, CDK4)
Inactivation of tumor suppressor genes (Rb, CDK inhibitor p16INK4a, p53)
Regulators of apoptosis (Bcl-2)
DNA repair genes (BRCA-1, BRCA-2, hMSH2)
-Growth Patterns of Malignant Neoplasms: Unregulated or uncontrolled growth, retain
capacity to replicate, usually don't differentiate to their mature counterparts
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