AOBPa Pathology cheat sheet

Coagulative necrosis: preserved tissue architecture with eosinophilic, anucleate cells; typical of ischemic infarction in heart, kidney, spleen.

Liquefactive necrosis: enzymatic digestion producing cystic cavity; characteristic of brain infarcts and abscesses.

Caseous necrosis: friable, structureless center with granulomatous rim; hallmark of tuberculosis and some fungal infections.

Fat necrosis: chalky white saponification from released lipases; seen in acute pancreatitis and breast trauma.

Fibrinoid necrosis: bright eosinophilic vessel wall deposits of fibrin and immune complexes; seen in vasculitis and malignant hypertension.

Apoptosis versus necrosis: apoptosis is energy-dependent, single-cell, non-inflammatory, with chromatin condensation and apoptotic bodies.

Metaplasia is a reversible change of one mature epithelial type to another; Barrett esophagus is columnar replacement of squamous mucosa.

Dysplasia denotes disordered growth with cytologic atypia but intact basement membrane; loss of basement membrane defines invasion.

Anion gap = Na − (Cl + HCO3); normal 8–12 mEq/L; elevated gap suggests ketoacidosis, lactic acidosis, uremia, or toxins.

Corrected sodium for hyperglycemia: add 1.6 mEq/L to measured Na for every 100 mg/dL glucose above 100.

Serum osmolality ≈ 2(Na) + glucose/18 + BUN/2.8; measured-to-calculated difference >10 suggests unmeasured osmoles.

Reticulocyte index = reticulocyte % × (patient hematocrit / normal hematocrit) / maturation correction; >2 indicates adequate marrow response.

Corrected calcium = measured Ca + 0.8 × (4.0 − albumin g/dL); low albumin lowers total but not ionized calcium.

FeNa = (urine Na × plasma Cr) / (plasma Na × urine Cr) × 100; <1% suggests prerenal azotemia.

Prothrombin time assesses extrinsic and common pathway (factors VII, X, V, II, fibrinogen); aPTT assesses intrinsic and common pathway.

Hemolysis in a specimen elevates potassium, LDH, and AST while lowering glucose; spuriously raises serum potassium.

Frozen section indications: intraoperative margin assessment, determination of metastasis, and identification of tissue (e.g., parathyroid).

Margins are reported as negative, positive (tumor at inked surface), or close; distance in millimeters should be stated when close.

Lymph node staging requires adequate sampling; sentinel node evaluation uses serial sectioning and cytokeratin immunohistochemistry.

Gross examination documents size in three dimensions, color, consistency, and relationship to margins and adjacent structures.

Tumor grading describes differentiation; staging describes anatomic extent and generally carries greater prognostic weight.

Specimen orientation and inking must occur before sectioning to allow accurate margin mapping.

Frozen section artifact includes ice crystal distortion and cautery artifact; avoid interpreting cauterized margins as positive.

Synoptic reporting follows standardized cancer protocols and includes margin status, lymphovascular invasion, and perineural invasion.

Bethesda System for cervical cytology: NILM, ASC-US, LSIL, ASC-H, HSIL, AGC, and carcinoma categories.

Koilocytes show perinuclear halo with nuclear enlargement, hyperchromasia, and wrinkling; indicate HPV cytopathic effect (LSIL).

Fine-needle aspiration yields cytologic material for mass triage; loss of architecture limits distinction of invasive from in situ disease.

Pap smear adequacy requires adequate squamous cellularity and transformation zone sampling when indicated.

Malignant effusions show cellular clusters with nuclear enlargement, high N/C ratio, and prominent nucleoli; immunocytochemistry aids origin.

Atypia of undetermined significance (AUS/FLUS) in thyroid FNA carries roughly 5–15% malignancy risk and often prompts repeat or molecular testing.

Cytology cannot reliably assess invasion; architectural invasion requires histologic evaluation of tissue.

Air-dried smears (Diff-Quik) highlight cytoplasmic and stromal features; alcohol-fixed smears (Pap) highlight nuclear detail.

Iron deficiency anemia: microcytic, low ferritin, high TIBC, low transferrin saturation, and elevated RDW.

Anemia of chronic disease: normocytic or microcytic with low TIBC, normal-to-high ferritin, and low transferrin saturation.

Thalassemia trait shows microcytosis with normal or high RBC count and normal ferritin; Mentzer index <13 favors thalassemia.

CML is defined by t(9;22) BCR-ABL1; peripheral smear shows leukocytosis with full myeloid maturation and basophilia.

Hodgkin lymphoma shows Reed-Sternberg cells (CD15+, CD30+, CD45−) in an appropriate inflammatory background.

Burkitt lymphoma shows t(8;14) MYC translocation, starry-sky histology, and high Ki-67 proliferation index.

Multiple myeloma criteria include clonal plasma cells ≥10%, M protein, and CRAB features (calcium, renal, anemia, bone lesions).

Flow cytometry immunophenotyping identifies lineage and clonality; CD5 and CD23 coexpression supports CLL/SLL.

PCR amplifies DNA exponentially through denaturation, annealing, and extension cycles; sensitivity allows detection of low-abundance sequences.

Sanger sequencing reads single amplicons; next-generation sequencing enables massively parallel interrogation of many genes.

FISH detects chromosomal rearrangements and amplifications using fluorescent probes; useful for translocations such as BCR-ABL1.

Germline variants are present in all cells and are heritable; somatic variants are confined to tumor tissue.

Variant classification uses tiers: pathogenic, likely pathogenic, variant of uncertain significance, likely benign, benign.

Loss of mismatch repair proteins (MLH1, PMS2, MSH2, MSH6) by immunohistochemistry suggests microsatellite instability.

EGFR, ALK, ROS1, and KRAS testing guide therapy selection in non-small cell lung carcinoma.

BRCA1/2 pathogenic variants confer increased risk of breast and ovarian carcinoma and inform PARP inhibitor eligibility.

Gram-positive cocci in clusters suggest Staphylococcus; in chains suggest Streptococcus.

Gram-negative diplococci in neutrophils suggest Neisseria; intracellular location is characteristic in gonococcal urethritis.

Granulomas with caseation suggest tuberculosis; noncaseating granulomas suggest sarcoidosis, Crohn disease, or fungal infection.

Special stains: acid-fast for mycobacteria, silver stains for fungi and Pneumocystis, mucicarmine for Cryptococcus capsule.

Abscess formation with neutrophils is typical of pyogenic bacteria; viral inclusions include Cowdry bodies (herpes) and Negri bodies (rabies).

Prion disease shows spongiform change, neuronal loss, and absence of inflammation; amyloid plaques may be present.

Cytopathic effect in cell culture includes rounding, syncytia formation, and inclusion bodies, aiding viral identification.

Sterile pyuria with negative routine cultures should prompt consideration of Chlamydia, Ureaplasma, or mycobacterial infection.

Somatic dysfunction is impaired or altered function of related components of the somatic system: skeletal, arthrodial, and myofascial structures and related vascular, lymphatic, and neural elements.

Tissue texture change, asymmetry, restriction of motion, and tenderness (TART) are the cardinal diagnostic criteria for somatic dysfunction.

Lymphatic congestion may accompany inflammatory and neoplastic processes; osteopathic lymphatic techniques are proposed to support drainage, not to treat malignancy.

Viscerosomatic reflexes produce segmental somatic findings corresponding to sympathetic innervation of an affected viscus.

Referred pain from visceral pathology follows shared spinal cord segments; cardiac ischemia may refer to the left shoulder and arm.

The body is a unit; structure and function are reciprocally interrelated; the body possesses self-regulatory mechanisms.

Osteopathic manipulative treatment is adjunctive and does not substitute for indicated biopsy, staging, or antimicrobial therapy.

Contraindications to manipulative treatment include unstable fractures, acute bony destruction from metastasis, and severe coagulopathy.