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Steps in scar formation

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Last updated

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Date created

Mar 1, 2020

Cards (79)

Section 1

(50 cards)

Steps in scar formation

Front

1. Angiogenesis 2. Fibroblast migration + proliferation 3. Maturation + reorganization of fibrous tissue

Back

melanoma

Front

skin cancer

Back

acute inflammation

Front

Minimal and short-lasting injury to tissue, mainly neutrophils

Back

physiological apoptosis examples

Front

loss of tissue between digits in embryonic development, removal of degenerate cells lining bowel

Back

Granulomatous inflammation

Front

-Macrophages mass together around foreign bodies, lymphocytes then surround macrophages -Connective tissue surrounds and isolates the mass, forming granuloma (but giant cells first)

Back

Wet gangrene vs dry gangrene

Front

caused by bacterial infection (area swells, drains fluid, smells bad) vs caused be lack of blood supply (area turns black, shrinks, is dry)

Back

caseous necrosis

Front

degeneration and death of tissue with a cheese-like appearance, associated with TB (microscope: eosinophilic centre surrounded by lymphocytes and macrophages, giant cells)

Back

Reversible cell injury

Front

ATP depletion, paralysis of ion pumps leading to H2O collecting within the cell leading to swelling, impaired oxidation of fatty acids, increased synthesis and uptake, liver secretes less VLDL

Back

epithelial metaplasia

Front

acquired tissue can withstand conditions better than previous tissue (refluxed gastric acid in oesophagus leads to squamous epithelia being replaced with columnar)

Back

Necrosis

Front

energy independent tissue death with inflammation

Back

Non-caseating granulomas

Front

associated with Crohn's disease, sarcoidosis, leprosy, reaction to foreign bodies (splinter)

Back

Steps in acute inflammatory response

Front

recognition, recruitment, removal, regulation, repair

Back

first intention

Front

mainly epithelial regeneration with minimal scarring

Back

pathological apoptosis examples

Front

cell damage due to viruses, tumours

Back

liposarcoma

Front

cancer of fatty tissue

Back

termination of inflammatory response

Front

decay of chemical mediators, inflammatory inhibitors, clearance if necrotic debris

Back

papillary cystadenoma

Front

Back

chronic inflammation

Front

severe and progressive tissue injury, mast cells macrophages, lymphocytes involved

Back

scar formation

Front

replacement of damaged cells with collagen

Back

hepatoma

Front

tumor of the liver

Back

Coagulative necrosis

Front

tissue necrosis in which component cells are dead but basic architecture is preserved for a short while (seen in every organ EXCEPT brain) (microscope: preserved cell with no nucleus)

Back

Fibromatosis

Front

also called desmoids tumor -> soft tissue tumor composed of proliferating fibroblast -> invade locally (dermal and subcutaneous) but do not metastasize

Back

physiological hyperplasia (hormonal)

Front

enlargement of breasts at puberty and pregnancy

Back

autolysis

Front

destruction of cells by enzymes within the cells

Back

teratoma

Front

a germ cell neoplasm made of several different differentiated cell/tissue types

Back

second intention

Front

wide gap of wound edges, more granulation tissue, more necrotic debris and fibrin, scarring

Back

adenocarcinoma

Front

malignant tumor of glandular tissue

Back

metaplasia

Front

Mature cell type is replaced by a different mature cell type

Back

hyperplasia vs hypertrophy

Front

increase in cell number vs increase in cell size

Back

seminoma

Front

testicular tumour

Back

Causes of granulomatous inflammation

Front

-persistent T-cell response to microbes leading to chronic macrophage activation -immune mediated disease -prolonged exposure to toxic agent

Back

rhabdomyosarcoma

Front

malignant skeletal muscle tumor

Back

connective tissue metaplasia

Front

the formation of cartilage, bone, or adipose tissue in tissues that normally do not contain it (myositis ossificans)

Back

physiological hypertrophy

Front

increase in skeletal muscle size due to exercise/ increase in cardiac muscle size due to increased demand (left ventricular hypertrophy in systemic hypertension)

Back

Apoptosis

Front

energy dependent death of single celk

Back

Liquefactive necrosis

Front

lipid rich tissue broken down by lysosomal enzymes into liquid mass (stroke in brain) (microscope: lots of neutrophils)

Back

Features of necrosis

Front

cytoplasmic membrane disruption/ cell swelling, lysosomal breakdown, phagocytosis, inflammatory response

Back

sarcoidosis

Front

autoimmune disease with fibrous lesions forming in lymph nodes, liver, skin, lungs, spleen, eyes, and small bones of hands and feet

Back

fibrosarcoma

Front

cancer of fibrous tissue

Back

leiomyosarcoma

Front

malignant smooth muscle tumor

Back

lymphoma

Front

malignant tumor of lymph nodes and lymph tissue

Back

apoptosis features

Front

chromatin condensation, cell shrinkage, cytoplasmic organelles in tact, no inflammatory response, fragmentation of nucleus and cytoplasm

Back

physiological hyperplasia (compensatory)

Front

liver hyperplasia after partial hepatectomy

Back

heterolysis

Front

Digestive enzymes from other cells break down dead cell

Back

mesothelioma

Front

rare malignant tumor arising in the pleura

Back

osteosarcoma

Front

bone cancer

Back

adenoma

Front

a benign tumor that arises in glandular tissue

Back

cystadenoma

Front

benign adenoma containing cysts

Back

Examples of granulomatous inflammation

Front

diabetes, pulmonary silicosis, TB, lupus, arthritis, cancer

Back

Formation of granulation tissue

Front

angiogenesis, fibroblast proliferation, loose connective tissue and immature collagen fibers

Back

Section 2

(29 cards)

cachexia

Front

loss of weight, profound weakness, anorexia associated with malignancy

Back

cicatrisation

Front

formation of a scar

Back

keloid

Front

excessive collagen production

Back

misnomers

Front

melanoma, lymphoma, seminoma, hepatoma, mesthelioma (these sound benign but are actually malignant)

Back

Proto-oncogenes

Front

normal cellular genes that are responsible for normal cell growth and division (these can mutate to form oncogenes which cause uncontrolled cell cycling)

Back

Front

Back

paraneoplastic syndrome

Front

Symptoms triggered by a cancer that cannot be explained

Back

sarcoma

Front

malignant tumor of connective tissue

Back

Characteristics of malignant phenotype

Front

evading apoptosis, no reaction to anti-growth signals, metastasis, sustained angiogenesis, continuous replication

Back

oncogenesis/carcinogenesis

Front

development of cancer

Back

tumor grade

Front

Degree of cellular differentiation based on histologic appearance of tumor

Back

Congenital carcinogenesis

Front

person inherits one defective copy of gene (APC, NF 1, Rb)

Back

BRCA1 and BRCA2

Front

breast cancer 1 and 2

Back

examples of carcinogens

Front

radiation, chemicals, microorganisms (Hep B, HTLV1, EBV), mutations

Back

carcinoma

Front

a cancer arising in the epithelial tissue

Back

helicobacter pylori

Front

causes stomach ulcers

Back

adenosarcoma

Front

malignant cancer of glandular origin

Back

schwannoma

Front

Benign tumor of Schwann cells

Back

examples of paraneoplastic syndromes

Front

polycythemia (seen with renal cell carcinoma), hypercalcemia (seen with squamous cell carcinoma of lung)

Back

enchondroma

Front

Benign tumor consisting of cartilage

Back

angiolipoma

Front

Tumor that contains numerous small blood vessels with fat

Back

tumour markers

Front

Substances produced by benign and malignant cells that can be monitored to show presence of malignant tissue

Back

dysplasia

Front

abnormal development of tissue

Back

hamartoma

Front

benign tumour caused by abnormal growth of normal cells in the area where they normally are

Back

granulation tissue

Front

the tissue that forms during the healing of a wound composed of immature collagen, fibroblasts and new capillaries

Back

choristoma

Front

normal tissue aberrant tissue location; pancreatic tissue stomach wall

Back

oncogenes

Front

genes that cause cancer by blocking the normal controls on cell reproduction and drive uncontrolled cell cycling

Back

Targets of genetic damage

Front

growth-promoting proto-oncogens, growth inhibiting tumour suppressor genes, genes that regulate apoptosis, genes involved in DNA repair

Back

tumour suppressor genes

Front

These keep the activity of proto-oncogenes in check in normal healthy cells (if defective, they cannot restrict cell cycling)

Back