patho unit 1 exam

types of cellular adaptation

atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia

what prompts cellular adaptation?

an appropriate stimulus

cell atrophy

a decrease in cell size

apoptosis

programmed cell death

causes of cell atrophy

disuse, denervation, loss of endocrine stimulation, inadequate nutrition, ischemia (decreased blood flow)

cell hypertrophy

increase in cell size/tissue mass

what kinds of cells typically undergo hypertrophy?

cardiac and skeletal muscle tissue

adaptive (to disease) hypertrophy

myocardial hypertrophy due to hypertension or thickening of bladder wall

compensatory hypertrophy

the enlargement of a remaining organ or tissue after a portion has been surgically removed or becomes inactive

initiating signals of hypertrophy

ATP depletion, mechanical forces, hormonal factors

cell hyperplasia

increase in the number of cells

what kind of tissue undergoes hyperplasia?

cells capable of undergoing mitotic division (NOT nerve, skeletal, or cardiac cells)

what controls hyperplasia?

gene activation

physiologic hyperplasia

hormonal stimulation or compensatory

metaplasia

the substitution of one cell type with another

dysplasia

deranged cell growth of a specific tissue that results in cells with variant size, shape, and appearance

which kind of cell adaptation is considered a precursor of cancer?

dysplasia

intracellular accumulations

buildup of substances that cells cannot immediately use or dispose of

where do intracellular accumulations accumulate

cytoplasm

types of substances that accumulate

normal body substances (lipids, proteins, melanin)

abnormal endogenous products 

exogenous products that can’t be metabolized (coal dust, tattoos) 

icterus

increase in bilirubin → jaundice

pathologic calcifications

abnormal tissue deposition of calcium salts alongside smaller amounts of iron, magnesium, and other minerals

dystrophic calcification

occurs in dead/dying tissue

metastatic calcification

occurs in normal tissue (hypercalcemia)

causes of cell injury

chemical injury, biologic agents, nutritional imbalances, physical agents, radiation

chemical injury of cell

drugs, mercury, lead

cell injury from biologic agents

viruses, parasites, bacteria

physical agents of cell injury

bodily impact, extreme temperatures, electricity

radiation injury of cell

UV, ionizing and non-ionizing radiation

hypoxic cell injury

oxygen deprivation of the cell which interrupts ATP generation

causes of hypoxia

inadequate amount of oxygen in the air, respiratory disease, edema, ischemia, cell inability to use oxygen

two patterns of reversible cell injury

cellular swelling and fatty change

what kinds of cells undergo apoptosis

cells that:

are worn out

have been produced in excess

have developed improperly

have genetic damage

necrosis

cell death in an organ or tissue that is still part of a living person

types of necrosis

liquefaction, coagulation, caseous

liquefaction

cells die but catalytic enzymes not destroyed (abscess)

coagulation

acidosis denatures the enzymatic and structural proteins of the cell (hypoxia)

caseous necrosis

tubercular lesions (immune reactions)

gangrene

occurs when a considerable mass of tissue undergoes necrosis

types of gangrene

dry, wet, and gas

dry gangrene

a type of coagulation necrosis that interferes with blood supply, HAS MARK OF DEMARCATION and a slow spread

wet gangrene

a type of odor liquefaction causes by bacterial infection or bedsores with NO DEMARCATIONS and rapid spread

gas gangrene

infection of clostridium perfringens that spreads gas in the tissue; occurs in trauma and compound fractures where dirt and debris are embedded

causes of birth defects

genetic factors, environmental factors, intrauterine factors

single-gene disorders

caused by a single defective or mutant gene

what pattern do birth defects follow?

medelian pattern

autosomal dominant

a single mutant allele from an affected parent is transmitted to an offspring regardless of sex

marfan syndrome

connective tissue disorder manifested by changes in the skeleton, eyes, and cardiovascular system. characterized by pigeon chest and kyphosis

neurofibromatosis

a condition where neurogenic tumors that arise from Schwann cells and other PNS elements

Huntington disease

progressive degenerations of neurons in the brain, usually sets in when patient is middle-aged

autosomal recessive

manifested only when both members of the gene pair are affected (both parents are carriers)

phenylketonuria (PKU)

metabolic disorder caused by a deficiency of the liver enzyme phenylalanine hydroxylate

Tay-Sachs Disease

a variant of a class of lysosomal storage disease, known gangliosidoses

sickle cell disease

single base change in globin gene changes 1 amino acid in hemoglobin and makes red blood cells sickle

cystic fibrosis

chloride ion channel defect causes abnormally thick mucus

X-linked recessive

x-linked disorders

hemophilia A, duchenne dystrophy

fragile X syndrome

fragile sire on X chromosome where chromatin fails to condense during mitosis and causes mental retardation

multifactorial inheritance disorders

cleft lip, clubfoot, congenital hip dislocation, congenital heart disease, pyloric stenosis, urinary tract malformation

results of chromosomal disorders

early gestational loss, congenital malformations, intellectual disability

types of chromosomal disorders

trisomy 21 (down syndrome), monosomy X (turner syndrome), polygamy X (Klinefelter syndrome)

teratogenic agents

radiation, chemicals and drugs, infectious agents

fetal alcohol syndrome

prenatal/postnatal growth retardation, CNS abnormalities

characteristics of fetal alcohol syndrome

short eye openings, thin upper lip, elongated, flattened mid face, and philtrum

TORCH

toxoplasmosis, other, rubella, cytomegalovirus, herpes

components of tissue renewal and repair

cell proliferation, cell differentiation, apoptosis

phases of cell cycle for neoplasms

4/5 of life cycle in mitosis and 1/5 of life cycle in other phases

categories of cell types

well differentiated neurons, skeletal muscle, cardiac muscle; parent cells that provide and reproduce; blood cells, skin cells, liver cells; undifferentiated stem cells

characteristics of benign neoplasms

inability to metastasize to distant sites, composed of well-differentiated cells that resemble the cells of the tissue of origin, a slow rate of growth, expansive manner of growth

malignant neoplasms

tend to grow rapidly and spread widely, have the potential to kill, compress blood vessels and outgrow blood supply, rob tissue of essential elements, liberate toxins that destroy tumor and normal tissue

methods by which cancer spreads

direct invasion/extension, seeding of cancer cells in body cavities, metastatic spread through blood or lymph

factors that affect tumor growth

number of cells actively dividing, duration of cell cycle, ratio of cells being lost to being produced, growth fraction, doubling time (length of time it takes for the total mass of cells in a tumor to double)

genes that control cell growth and replication

protooncogenes, tumor suppressor genes, genes that control apoptosis, genes that regulate repair of damaged DNA

steps of turning normal cells into cancer cells

cells exposed to carcinogenic agents, unregulated accelerated growth in initiated cells, tumor cells acquire changes that promote invasiveness, autonomous growth

environmental factors leading to cancer

heredity, hormones, carcinogens, stem cells

staging of tumors

how large is the tumor? have cancer cells spread to regional lymph nodes? has the cancer spread to other regions of the body?

cancer treatment modalities

surgery, radiation, hormone therapy, biotherapy, chemotherapy

goals of cancer treatment

curative, control, palliative