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Block 1 threads > Histopathology > Flashcards

Histopathology Flashcards

1
Q

Cell adaptationsto stress/or death

atrophy

A

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

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2
Q

Cell adaptationsto stress/or death

hypertrophy

A

cells increase size to repsond to functional demands. Additional organelles and Plasma M. added. HISTOLOGICALLY:

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3
Q

Cell adaptationsto stress/or death

hyperplasia

A

increased number of cells/proliferation of cells. Can be precancerous. HISTOLOGICALLY: more cells

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4
Q

Cell adaptationsto stress/or death

metaplasia

A

cells become different differentiated cells.

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5
Q

Cell adaptationsto stress/or death

Barret’s esophagus

A

Ex of metaplasia: esophagus epithelium become more like stomach epithelium as a result of chronic acid reflux

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6
Q

Cell adaptationsto stress/or death

Apoptosis

A

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

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7
Q

Cell adaptationsto stress/or death

pyknosis

A

darkly basophilic condensed nucleus (occurs in both apoptosis and necrosis). Early stage of dying cell

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8
Q

Cell adaptationsto stress/or death

necrosis

A

dead or dying cells. Pathologic and inflammatory by definition. 2 types (1) coagulative (2) liquifactive

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9
Q

Cell adaptationsto stress/or death

coagulative necrosis

A

(protein denaturation). Results from hypoxic or ischemic damage. HP: tissue architecture intact, nucleus faded or absent, eosiniphilic (protein and lack of RNA)

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10
Q

Cell adaptationsto stress/or death

liquifactive necrosis

A

(enzyme digestion). bacterial infections with inflammation- release of lysosomal contents by immune cells kills other cells. HP:cell architecture lost

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11
Q

Neoplasia

A

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

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12
Q

Benign tumor

A

Tumor that is still in the tissue compartment it “belongs” in

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13
Q

Malignant tumor

A

Tumor that has infiltrated adjacent and/or distant tissue compartments that is does not “belong” in

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14
Q

Genetic defects causing a cell to become neoplastic

A

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

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15
Q

Architecture

A

The way cells are arranged in relation to each other (big picture)

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16
Q

Cytology

A

Examination of nuclear features and the nuclear:cytoplasmic ratio

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17
Q

Dysplasia

A

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

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18
Q

Carcinoma In Situ

A

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

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19
Q

Histological features of malignant neoplasms

A

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

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20
Q

Anaplasia

A

Cell no longer recognizable as a cell from its tissue origin; de-differentiated cells

Not a good prognosis

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21
Q

Metastasis

A

Process by which tumor cells migrate away from their compartment of origin and colonize distant compartments

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22
Q

Mutations that lead to metastasis

A

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

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23
Q

Where do metastatic carcinomas end up? Why?

A

Regional lymph nodes

Because lymphatic vessels constantly drain extracellular fluid, so anything not firmly attached to the extracellular matrix will enter lymphatic circulation

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24
Q

Where do sarcomas (derived from mesoderm) metastasize to?

A

Blood vessels

25
Q

Benign neoplasm

A

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

26
Q

Can benign neoplams be dangerous?

A

Yes, if they obstruct or compress other structures

27
Q

Carcinoma

A

Tumor of epithelial origin

28
Q

Basal cell carcinoma

A

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

29
Q

Adenocarcinoma

A

Malignant tumor of gland cells

30
Q

Sarcoma

A

Tumor of mesenchymal origin (connective tissues)

31
Q

Fibrosarcoma

A

Malignant tumor of fibroblasts

32
Q

Liposarcoma

A

Malignant tumor of adipocytes

33
Q

Osteosarcoma

A

Malignant tumor of bone cells

34
Q

Adenoma

A

Benign tumor of gland cells

35
Q

Fibroma

A

Benign tumor of fibroblasts

36
Q

Lipoma

A

Benign tumor of adipocytes

37
Q

Osteoma

A

Benign tumor of bone cells

38
Q

Leiomyoma

A

Benign tumor of smooth muscle

39
Q

From the name, how can you tell if a neoplasm is malignant or benign?

A

Malignant has “carcinoma” or “sarcoma” suffix

Benign just has “oma” suffix

40
Q

TNM system

A

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

41
Q

Histological appearance of acute inflammation

A

Many neutrophils, usually macrophages, sometimes eosinophils

Lymphocytes as well, but those are in both acute and chronic inflammatory responses

42
Q

Neutrophils

A

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

43
Q

Eosinophils

A

Multilobed nucleus sometimes hard to see

Bright pink granules

Seen in parasitic infection, asthma, allergic reaction

A few eosinophils at site of acute inflammation

44
Q

Basophils

A

Cannot see nucleus b/c of basophilic granules

Dark basophilic granules

Functions similar to mast cells

Rarest type of granulocyte

45
Q

Macrophoages (aka Histiocytes)

A

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

46
Q

Macrophage names for other tissues

A

Lanterhans cell in skin

Kupffer cell in liver

Dust cell in lungs

Sinus histiocytes in spleen

Microglia in brain

47
Q

Lymphocytes

A

In both acute and chronic inflammation

Large, round basophilic nuclei

48
Q

Suppurative inflammation/Abcess

A

What we have previously referred to as liquifactive necrosis

Pus is formed

49
Q

Serous inflammation

A

Large white spaces due to abundance of exudate can disfigure architecture of tissue

Grossly, can present as blister filled with pus

50
Q

Fibrinous inflammation

A

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

51
Q

How are macrophages involved in tissue remodeling and repair?

A

They stimulate fibroblasts and endothelial cells to proliferate in order to rebuild tissue stroma

52
Q

Fibrosis

A

Macrophages during chronic inflammation create fibrosis

Synthesis of new collagen as a result of chronic inflammation

53
Q

Granulomatous inflammation

A

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

54
Q

Lymphoid tissues (tissues composed of lymphocytes)

A

Follicle-based appearance, dark area of T cells (marginal zone) around light central area of B cells, and dendritic cells everywhere

55
Q

Collections of lymphocytes that do NOT have follicle arrangement

A

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

56
Q

Squamous cell carcinoma

A

Histology: contains keratin pearls

On skin surface: crevace/crater in skin

57
Q

Hyperkeratosis

A

Thick keratin layer

58
Q

Parakeratosis

A

Nucleated cells in keratin layer

Block 1 threads (4 decks)

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