Histopathology Flashcards
Cell adaptationsto stress/or death
atrophy
process by which cells decrease in size by digesting some of their intracellular machinery in order to attain a lower energy requirement status. Results from (1) lack of nutritional supply for some time (2) denervation of muscle cells (3) cells have been inactive for prolonged temporal period. HISTOLOGICALLY: cells are smaller
Cell adaptationsto stress/or death
hypertrophy
cells increase size to repsond to functional demands. Additional organelles and Plasma M. added. HISTOLOGICALLY:
Cell adaptationsto stress/or death
hyperplasia
increased number of cells/proliferation of cells. Can be precancerous. HISTOLOGICALLY: more cells
Cell adaptationsto stress/or death
metaplasia
cells become different differentiated cells.
Cell adaptationsto stress/or death
Barret’s esophagus
Ex of metaplasia: esophagus epithelium become more like stomach epithelium as a result of chronic acid reflux
Cell adaptationsto stress/or death
Apoptosis
programmed cell death. non-inflammatory. physiological or pathological. apoptotic bodies sent out to by phagocytized by macrophages. T-cells instruct self-termination. HP: hard to find. (1) pyknosis (2) extrusion (3) eosinophilic (4) karryohexis
Cell adaptationsto stress/or death
pyknosis
darkly basophilic condensed nucleus (occurs in both apoptosis and necrosis). Early stage of dying cell
Cell adaptationsto stress/or death
necrosis
dead or dying cells. Pathologic and inflammatory by definition. 2 types (1) coagulative (2) liquifactive
Cell adaptationsto stress/or death
coagulative necrosis
(protein denaturation). Results from hypoxic or ischemic damage. HP: tissue architecture intact, nucleus faded or absent, eosiniphilic (protein and lack of RNA)
Cell adaptationsto stress/or death
liquifactive necrosis
(enzyme digestion). bacterial infections with inflammation- release of lysosomal contents by immune cells kills other cells. HP:cell architecture lost
Neoplasia
Used interchangeably with “tumor” and “cancer” but can be either benign or malignant
Caused by accumulation of:
1) inherited genetic mutations
2) environmentally acquired genetic mutations
Benign tumor
Tumor that is still in the tissue compartment it “belongs” in
Malignant tumor
Tumor that has infiltrated adjacent and/or distant tissue compartments that is does not “belong” in
Genetic defects causing a cell to become neoplastic
All promote additional defects:
1) cause cell to enter cell cycle more frequently
2) diminish normal inhibition of replication for cell
3) diminish or abolish apoptotic ability
4) impair ability to repair DNA
5) abolish cell senescence
Architecture
The way cells are arranged in relation to each other (big picture)
Cytology
Examination of nuclear features and the nuclear:cytoplasmic ratio
Dysplasia
Cells still reside in correct compartment (not malignant) but have acquired some genetic defects and no longer look or behave quite right
Examples: cells or nuclei have abnormal polarity, tissue architecture disordered or layers not recognizable, cell nuclei abnormally shaped
Carcinoma In Situ
Only epithelial cells and NOT malignant; whole epithelium is somehow deranged: “full thickness dysplasia”
Few if any normal cells remaining, so very close to achieving malignancy
Histological features of malignant neoplasms
1) abundant mitotic figures
2) irregular borders
3) limbs or branches of tumor cells leading outward from center of lesion
4) center of fast growing tumor can be necrotic (tumor’s appetite for nutrition outstripped what is available)
5) inflammatory cells (especially necrotic tumors)
6) darker basophilic staining because nuclear:cytoplasmic ratio is high
7) can bleed because they stimulate angiogenesis but new vessels are not formed very well so they’re “leaky”
8) disordered and messy architecture
9) heterogenous nuclear appearances
Anaplasia
Cell no longer recognizable as a cell from its tissue origin; de-differentiated cells
Not a good prognosis
Metastasis
Process by which tumor cells migrate away from their compartment of origin and colonize distant compartments
Mutations that lead to metastasis
1) adherence of cell to neighboring cells and/or basement membrane
2) regulate cells expression to extracellular matrix, allowing cell to “crawl”
3) control expression of enzymes that break down extracellular matrix allowing cell to create a route to move through
Where do metastatic carcinomas end up? Why?
Regional lymph nodes
Because lymphatic vessels constantly drain extracellular fluid, so anything not firmly attached to the extracellular matrix will enter lymphatic circulation
Where do sarcomas (derived from mesoderm) metastasize to?
Blood vessels
Benign neoplasm
Tumors that are not a metastatic threat
1) slow growing
2) well defined borders and/or encapsulated (white on H&E stain)
3) few mitotic figures
4) well differentiated
Can benign neoplams be dangerous?
Yes, if they obstruct or compress other structures
Carcinoma
Tumor of epithelial origin
Basal cell carcinoma
Type of malignant skin cancer (does not metastasize)
Histology: cystic pattern with pockets of light purple staining surrounded with dark basophilic staining
On skin: pearly pink papule
Adenocarcinoma
Malignant tumor of gland cells
Sarcoma
Tumor of mesenchymal origin (connective tissues)
Fibrosarcoma
Malignant tumor of fibroblasts
Liposarcoma
Malignant tumor of adipocytes
Osteosarcoma
Malignant tumor of bone cells
Adenoma
Benign tumor of gland cells
Fibroma
Benign tumor of fibroblasts
Lipoma
Benign tumor of adipocytes
Osteoma
Benign tumor of bone cells
Leiomyoma
Benign tumor of smooth muscle
From the name, how can you tell if a neoplasm is malignant or benign?
Malignant has “carcinoma” or “sarcoma” suffix
Benign just has “oma” suffix
TNM system
Method for staging tumors where 0 is best outcome and 4 is worst
T: severity of primary tumor
N: number of regional lymph nodes with metastases
M: number of distant metastases
Histological appearance of acute inflammation
Many neutrophils, usually macrophages, sometimes eosinophils
Lymphocytes as well, but those are in both acute and chronic inflammatory responses
Neutrophils
Prominent multilobed nuclei
Granules stain poorly and somewhat eosinophilic (pink) with H&E
First to arrive to site of acute inflammation (minutes to hours) then become more sparse (die after 2 days via apoptosis)
Phagocytose bacteria and/or dead cells and release antibacterial and antiviral products from granules
Dead neutrophils make up pus/abcess
Eosinophils
Multilobed nucleus sometimes hard to see
Bright pink granules
Seen in parasitic infection, asthma, allergic reaction
A few eosinophils at site of acute inflammation
Basophils
Cannot see nucleus b/c of basophilic granules
Dark basophilic granules
Functions similar to mast cells
Rarest type of granulocyte
Macrophoages (aka Histiocytes)
Arrive after neutrophils (24 hours after peak neutrophil activity)
Large cells with paler nuclei and white phagocytic vacuoles in cytoplasm
Phagocytic
Circulate in bone marrow as monocytes, before getting to tissue
Macrophage names for other tissues
Lanterhans cell in skin
Kupffer cell in liver
Dust cell in lungs
Sinus histiocytes in spleen
Microglia in brain
Lymphocytes
In both acute and chronic inflammation
Large, round basophilic nuclei
Suppurative inflammation/Abcess
What we have previously referred to as liquifactive necrosis
Pus is formed
Serous inflammation
Large white spaces due to abundance of exudate can disfigure architecture of tissue
Grossly, can present as blister filled with pus
Fibrinous inflammation
Occurs on a free surface within body cavity (pericardium)
Results from prolonged endothelial cell retraction that permits large proteins such as fibrin to accumulate at injury site
Plasma leaks into injured tissue and clots, forming fibrin
Worst kind of inflammation
Eosinic material deposited on surface
How are macrophages involved in tissue remodeling and repair?
They stimulate fibroblasts and endothelial cells to proliferate in order to rebuild tissue stroma
Fibrosis
Macrophages during chronic inflammation create fibrosis
Synthesis of new collagen as a result of chronic inflammation
Granulomatous inflammation
Cytoplasmic/light eosinophilic appearance, abundant nuclei, giant cells, surrounding “collar” of lymphocytes
When macrophages encounter particle/microbe they cannot degrade, they surround it and form a granuloma
Ex: TB, Syphilis, Sarcoidosis, Cat-scratch disease, foreign body reactions
Lymphoid tissues (tissues composed of lymphocytes)
Follicle-based appearance, dark area of T cells (marginal zone) around light central area of B cells, and dendritic cells everywhere
Collections of lymphocytes that do NOT have follicle arrangement
Mucosal Associated Lymphoid Tissue (MALT)
Gut Associated Lymphoid Tissue (GALT)
Bronchus Associated Lymphoid Tissue (BALT)
Mixture of T and B cells plus macrophages and/or dendritic cells
Squamous cell carcinoma
Histology: contains keratin pearls
On skin surface: crevace/crater in skin
Hyperkeratosis
Thick keratin layer
Parakeratosis
Nucleated cells in keratin layer
