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NBME PATHOLOGY EXAM 1 2025/2026 SPRING SUMMER QUESTIONS AND ANSWERS GRADED A+

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NBME PATHOLOGY EXAM 1 2025/2026 SPRING SUMMER QUESTIONS AND ANSWERS GRADED A+

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NBME PATHOLOGY EXAM



NBME PATHOLOGY EXAM 1 2025/2026 SPRING-
SUMMER QUESTIONS AND ANSWERS GRADED
A+


This type of necrosis features cell shape and organ structure preservation
due to coagulation of proteins
Coagulative necrosis




Where is coagulative necrosis seen?
Wedge shaped infarcts of solid organs


NOT the Brain or Pancreas




This type of necrosis features enzymatic lysis of cells and proteins due
to release of neutrophil enzymes
Liquefactive




When is liquefactive necrosis seen?

,NBME PATHOLOGY EXAM


Brain infarcts


Abscesses


Pancreatitis




This type of necrosis is characterized by a coagulative necrosis that
resembles tissue mummification (dry form), commonly involving the
lower extremities and GI tract.


Superimposed Liquefactive necrosis leads to the "wet" form.
Gangrenous




This type of necrosis is a combination of coagulative and liquefactive
necrosis that results in a "cottage cheese" like appearance of the affected
tissue.
Caseous Necrosis




When is Caseous Necrosis seen?

,NBME PATHOLOGY EXAM


Most characteristic of granulomatous inflammation in the lungs due to
TB or fungal infection




This form of necrosis leads to the chalky white appearance of adipose
tissue due to the deposition of calcium in saponified fat.
Fat necrosis




When is fat necrosis seen?
Trauma to the breast and Acute Pancreatitis




This form of necrosis is characterized by leakage of protein into blood
vessel walls.
Fibrinoid




When is fibrinoid necrosis seen?
1. Malignant HTN
2. Vasculitis

, NBME PATHOLOGY EXAM




What type of hypersensitivity reaction is Fibrinoid necrosis?
Type III




What is Apoptosis?
Energy (ATP) dependent cell death. The dying cell shrinks and nucleus
condenses / fragments in an organized manner.


(eosinophilic cytoplasm and basophilic nucleus)




Describe the intrinsic pathway of activation (Caspase-Apoptosis)
Occurs in response to cellular injury that inactivates BCL2.


This allows Cytochrome C to leak out of the mitochondria and activate
caspases to chop up the cell




Describe the extrinsic pathway of activation (Caspase-Apoptosis)

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