PC1 U2L3

pathology

the scientific study of the nature, origin, progress and cause of disease

Rudolf Ludwig Karl Virchow

the father of modern pathology

virchow’s node

enlarged left supraclavicular lymph node seen in metastatic cancer

Virchow’s triad

factors that predispose to thrombosis:

• endothelial injury

• altered blood flow

• blood hypercoagulability

labile cells

cells that can multiply and get replaced throughout life (skin)

stable cells

cells that can proliferate in response to an external stimulus like injury (liver)

permanent cells

cells that do not multiply in post natal life and therefore injury makes a scar and is irreversible (heart)

cell adaptation, cell death, cell injury

examples of cell changes

hypertrophy

increased cell/organ size

hyperplasia

increased number of cells

atrophy

decreased size of cell/organ, ex is disuse

metaplasia

change of one cell type to another

dysplasia

abnormal tissue development

cell injury

reversible and irreversible, secondary to hypoxia, infections, autoimmune disease, physical agents (trauma, radiation, temperature changes), aging

apoptosis

individual cell death

pyknosis

nucleus shrinks and appears very basophilic

karyorrhexis

nucleus breaks up and finally disappears

infaction

tissue death secondary to loss of arterial supply or venous drainage from an organ

necrosis

changes that accompany cell death and are due to the effects of enzymes on the injured cell

liquefactive necrosis

the dead cells get digested and form a collection of liquid (brain infarct)

gangrenous necrosis

cell necrosis secondary to loss of blood supply

dry gangrene

no secondary infection, type of gangrene

wet gangrene

secondary infection present, type of gangrene

caseous necrosis

dead tissue has a cheesy yellow-white appearance

fat necrosis

fat destruction, type of necrosis

acute inflammation

leukocyte (neutrophil) response to foreign agent/injury

rubor (redness), calor (warmth), dolor (pain), tumor (swelling)

cardinal signs of inflammation

1. margination to sides of vessel wall via selectins

2. adhesion to endothelial cells via integrins

3. transmigration through vessel wall

4. chemotaxis to site of injury

steps of leukocytes in inflammation

1. organism is inhaled

2. goes via trachea to bronchi and finally to alveoli

3. usually affects lower lobe or right middle lobe

4. host responds with acute inflammatory response (neutrophils)

5. alveolar debris is removed by macrophages

pneumonia steps

lobar pneumonia

acute inflammation present in an entire lung lobe

bronchopneumonia

patchy acute inflammation in lung around bronchi and bronchioles causing patchy areas of consolidation, often bilateral

chronic inflammation

lymphocytes, plasma cells, monocyte/macrophage, response to foreign agent/injury

granulomatous inflammation

type of chronic inflammation where macrophages and epithelioid histiocytes aggregate and together with giant cells and lymphocytes make a granuloma

caseating granuloma

granuloma that has central necrosis

non-caseating granuloma

type of granuloma that does not have central necrosis

tuberculosis, fungal infections, berylliosis, lymphoma, sarcoidosis

differential dx of granulomatous inflammation

edema

accumulation of fluid in extracellular spaces

starlings’ forces

maintain fluid equilibrium between blood vessel and interstitium - balance between hydrostatic pressure and plasma oncotic pressure

congestion

local increase in volume of blood to a particular organ or tissue

embolism

material that dislodges from it’s primary site of attachment and goes to a distal site

venous emboli

arise in veins commonly from lower extremity and tend to lodge in lungs

arterial emboli

arises from a mural thrombus in the heart and then lodge in distant organs such as the brain or lower extremities

paradoxic embolus

embolus from venous system enters arterial system via atrial septal defect or ventricular septal defect

saddle embolus

deep vein thrombosis in legs may dislodge, travels to right side of heart and into pulmonary arteries, if very large can occlude main pulmonary artery at bifurcation, resulting in sudden death

fat embolism

fat particles from long bones enter the circulation following a fracture of a long bone

air embolism

air enters circulation following chest wall injury or a surgical procedure or in decompression sickness (occurs in deep sea divers who ascend too rapidly, nitrogen bubbles get deposited in joints (bends) or lungs (chokes))

amniotic fluid embolism

serious obstetric complication where amniotic fluid enters maternal circulation and can cause a serious condition where disseminated intravascular coagulation - high mortality rate

tissue repair

restoration of tissue to the way it was prior to injury

regeneration, scar formation

types of tissue repair

regeneration

damaged tissue is repaired by organ and returns to normal state

scar formation

connective fibrous tissue is laid down in damaged area and repairs the tissue

cutaneous wound healing

occurs secondary to the formation of granulation tissue which is composed of connective tissue and blood vessels

healing by first intention

healing of a clean, incised wound (surgical incision)

healing by second intention

occurs in much larger wounds where a larger amount of granulation tissue is formed and the scar contracts, causing wound contraction

nutritional deficiency, keloid

wound healing complications

keloid

a condition which appears to be inherited where exuberant amount of connective tissue is formed which gives rise to raised scars

neoplasia

excessive uncoordinated growth of cells

hamartoma

benign mass composed of tissue native to the area in which the hamartoma is identified

heterotropic rest (choristoma)

benign mass composed of tissues not native to the area where it is present

carcinoma

malignant tumor of epithelial origin

adenocarcinoma

tumor arising from epithelial glandular tissue

squamous cell carcinoma

tumor arising from epithelial squamous cells, lining organs

sarcoma

malignant tumor of mesenchymal tissue

melanoma

malignant tumor of melanocytes

lymphoma

malignant tumor of lymphoid tissue

small cell carcinoma

typically in lung, small cells

teratoma

tumor composed of tissues arising from more than one germ cell layer, ectoderm, endoderm, mesoderm

oncogenes

genes that promote autonomous growth of cells

chemical carcinogens, radiation, viruses, bacteria

etiology of neoplasia

paraneoplastic syndromes

sx occurring secondary to a tumor (Cushing syndrome)

hx and physical exam, tumor markers, biopsy and cytology and needle aspiration, molecular dx

dx of neoplasia

tumor markers

measurable biochemical substances in the blood or urine that may indicate the presence of a tumor

prostate specific antigen (PSA)

may indicate prostate cancer if elevated - has low sensitivity and low specificity

carcinoembryonic antigen (CEA)

increased in cancers of colon, pancreas, stomach and breast - useful to detect cancer recurrence

tumor differentiation

the degree to which the tumor cells resemble the cell of origin

well differentiated tumor

cell of origin easily recognizable

moderately differentiated

between well differentiated and poorly differentiated

poorly differentiated

cell of origin cannot be easily recognized

curative/palliative, surgery, chemotherapy, radiation therapy, immunotherapy

cancer treatment

size of primary tumor, presence of nodal involvement, presence of metastatic disease

staging of tumors