Pathophysiology chapter 2

What are the 4 ways cells can adapt

What are the 4 ways cells can adapt

atrophy, hypertrophy, hyperplasia, metaplasia

__ is not true cellular adaption

dysplasia

Organs in where atrophy is more common

heart, skeletal muscles, secondary sex organs, brain

decrease in cell size

atrophy

atrophy physiologically occurs in the __

thymus

pathological causes of cell atrophy

decrease in workload, pressure, use, blood supply, nutrition

Atrophied muscle cells contain less

mitochondria, ER, myofilaments

In atrophy amino acid reuptake is

reduced

what is an increase in cell size

hypertrophy

Pregnancy can cause __ of the cardiac muscle

hypertrophy

Pathological causes of hypertrophy

hypertension, problematic valves, accumulation of proteins in cell compartments

Cell adaption where an increased number of mitotic division triggers DNA synthesis

hyperplasia

hyperplasia often occurs along with

hypertrophy

hyperplasia will not occur in

cardiac muscle

2 types of physiological hyperplasia

compensatory and hormonal

compensatory hyperplasia

allows organs to regenerate

hormonal hyperplasia

replaces lost tissue and encourages new growth, occurs in estrogen dependent organs

pathological hyperplasia can occur

after menopause

cell adaption from one type of mature cell type to a less mature cell

metaplasia

What happens in GI tract metaplasia after acid reflux

squamous cells are replaced by columnar cells

t/f metaplasia is reversible if the trigger is removed or lessened

true

metaplasia if often connected to

tissue damage, repair, and regeneration

t/f dysplasia is true cellular adaption

false

t/f dysplasia always indicates cancer

false

two places where dysplastic changes are frequently found

cervical and respiratory epithelial tissue

dysplasia is often associated with

neoplastic growths adjacent to cancer

atypical hyperplasia in breast tissue is a strong indicator of

breast cancer

t/f if inciting stimulus is removed dysplasia can be reversed

true

some types of cellular injury include

necrosis, apoptosis, pathological calcification, reversible, irreversible, active cell injury

which is worse for the surrounding cells apoptosis or necrosis

necrosis

causes of cellular injury

hypoxia, reperfusion injury, free radicals, toxic chemicals, infectious agents, physical and mechanical factors, immunologic reaction, genetic factors, nutritional imbalances, physical trauma

the most common type of cellular injury

hypoxia

cellular injury caused by lack of oxygen, loss of hemoglobin, leads to ischemia and inflammation

hypoxia

massive amounts of superoxide and peroxide, possibly caused by ishcemia, leads to pH changes, gap junction changes, Calcium overload, and even cell death

reperfusion injury

one unpaired electron that ellicits bond damage in proteins lipids and carbohydrates

free radical cell damage

cell damage from carcinogenic and mutagenic chemicals

toxic chemical cell damage

altering nucleus and plasma membrane via immune and inflammatory pathways

infectious agent cell injury

cell damage from climate change, temperature change, atomspheric pressure changes, ionizing radiation, or noise

physical and mechanical cell injury

steps to cell injury that lead to cell death

atp depletion, failure of active transport mechanisms, cellular swelling, detachment of ribosomes, cessation of protein synthesis, vacuolation, leakage of digestive enzymes, lysis of plasma membrane, death

atp depletion step

sodium influx with cellular swelling because atpase pump is no longer working,

failure of active transport

increased intracellular sodium and calcium, activation of enzymes that damage membrane protein atp and nucleic acids

cellular swelling step

influx of water due to influx of sodium

detachment of ribosomes

detachment of ribosomes from endoplasmic reticulum due to calcium influx

cessation of protein synthesis

caused by mitochondrial swelling from calcium accumulation

vacuolation

lysosome swelling, formation of vacuole in cytoplasm

leakage of digestive enzymes from lysosomes

autodigestion of intracellular structures

ischemia-reperfusion injury caused by

oxidative stress, free radicals damage membrane, mitochondrial pores open

effect of radicals on mitochondria

dysfunction and decreased antioxidants

chemical injury of the cell usually happens to the

plasma membrane

carbon monoxide

colorless and odorless gas that produces hypoxic injury, reduces oxygen carrying capacity of hemoglobin

carbon tetrachloride

common in dry cleaning, produces free radicals that damage p-450 enzyme

lead exposure

causes learning and behavior problems in children, speech and hearing problems, brain and nervous system damage, slowed growth development, kidney problems

treatment of lead

chelation therapy

ethanol cell damage

results in folate deficiency

ethanol is metabolized in

the liver

t/f up to a certain point ethanol can have a protective effect on cardiovascular system

true

acute alcoholism affects___ chronic alcoholism effects

CNS, liver and stomach

two major mercury sources

fish and healthcare equipment

sharp force injury

cutting or piercing

incised wound

longer than deep, no tissue bridging or undermining

stab wounds

deeper than long

puncture wounds

sharp point without sharp edges

chopping wound

crushed edges caused by sharp and blunt forces

contact range entrance wound

imprint of muzzle seen on skin

intermediate range entrance

under 48 inches, stippling of gun powder seen on skin

shored exit wound

caused if victim was wearing tight clothes or sitting againt a chain

asphyxial injury types

suffocation, strangulation, chemical, drowing

suffocation injury

oxygen failed to reach the blood

strangulation injury

compression of vessels and air passageway

chemical asphyxiants

block oxygen delivery

drowing

alteration of oxygen delivery by breathing in fluid

infectious injury

invasion and destruction caused by microorganism

immunologic and inflammatory injuries caused by

phagocytic cells

immune and inflammatory substances

histamines, antibodies, lymphokines, cytokines

injurous genetic and epigenetic factors

alterations in nucleus, plasma membrane structure, shape, receptors and mechanisms

injurious nutrition imbalances

deficient or excessive intake

temperature extreme injury

hypothermia, heat cramps, heat exhaustion, heat stroke, burns

treatment of heat cramps and heat exhaustion

treat with sodium and water

heat stroke

rectal temperature over 106 life threatening peripheral vasodilation

sudden infant death syndrome can be caused by

overheating

tissue injury caused by compression waves followed by sudden decompression

blast injury

carbon dioxide and nitrogen form gas emboli caused by water pressure being reduced too quickly

decompression sickness

types of high altitude illness

High altitude pulmonary edema and cerebral edema

any form of radiation capable of removing orbital electrons from ions can damage DNA in G2 phase

ionizing radiation

when cells not directly in the radiated field are affected by radiation, also know as horizontal transmission

bystander effects

generations of cells derived from an irradiated progenitor cell, lethal and nonlethal mutations appear

genomic instability

fluorescent lighting or excessive light exposure causes headache, eyestrain, eye discomfort

illumination injury

overexertion disorders of upper extremities and lower back, when mechanical forces exceed unknown thresholds

mechanical stresses

acoustic trauma and hearing loss can be caused by

noise damage

occurs when cell attempt to catabolize ‘stored’ substances that can cause metabolite accumulation

cellular accumulation disease

water storage disorder

cellular swelling by hypoxic injury

lipid and carbohydrate accumulation disease

abnormal accumulation in cells

glycogen accumulation disorder

occur in genetic conditions or conditions that affect glucose and glycogen metabolism

glycogen accumulation disorders can result in

excessive vacuolation and cell death

the point of no return for cell injury

calcium influx

2 ways accumulation of protein cause cell damage

metabolites produce toxic enzymes that damage organelles, amounts of proteins in cytoplasm push against organelles

What type of pigments are amino acids, melanin, blood proteins, porphyrins, hemoglobin, hemosiderin/ferritin, lipid rich pigment lipofuscin

endogenous

Examples of exogenous pigments

silica, iron, lead, silver, tattoo dyes,

the most common endogenous pigments

melanin, hemoproteins, bilirubin

hemoproteins are necessary for

iron storage