Cellular Adaptations and Necrosis

cell membrane

outer membrane that controls movement in and out

nucleus

controls cell division

ribosomes

site of protein synthesis

endoplasmic reticulum

folding and transport of proteins and lipids

lysozomes

contains enzymes that digest other cells or self

mitochondria

Powerhouse of the cell, organelle that is the site of ATP (energy) production

golgi complex

processes and packages proteins

temporary

cellular adaptations to pathologic conditions are usually _____. sever or long term stressors commonly overwhelm the adaptive processes resulting in cellular injury or death

immune response

prepares the body to fight infection

fever

raising body temperature impairs the replication of viruses and function of bacteria

signs

objective evidence of the disease

- skin rash or a cough

symptoms

Subjective characteristics of disease felt only by the patient

- stomach pain, back pain, fatigue

- other people only know about them if informed by that individual

syndrome

a group of signs and symptoms

diagnosis

Identification of an injury or disease

prognosis

the anticipated or expected course or outcome

prevalence

fraction of a population having a specific disease at a given time

incidence

The number or rate of new cases of a particular condition during a specific time.

atrophy

decrease in cell size

atrophic

if enough cells are affected the organ shrinks

skeletal/cardiac muscle and brain

what organs are most commonly atrophic?

physiologic atrophy

occurs with early development and is considered normal

- thymus (around age 10), ovaries after menopause

pathologic atrophy

occurs as a result of decreases in workload, pressure, use, blood supply, nutrition, hormonal stimulation, and nervous stimulation

- muscle atrophy (cast) and old age

hypertrophy

increase in cell size

response to mechanical load or stress, may increase the size of a whole organ

- often caused by repetitive motion/stretching, chronic pressure, and volume overload

- EX: muscle enlargement

physiologic hypertrophy

increased demand (strength training)

pathologic hypertrophy

underlying disease (hyperthyroidism --> goiter)

hyperplasia

increase in number of cells due to increased cell division

physiologic compensatory hyperplasia

mechanism that enables organs to regenerate

- skin, liver, intestines, etc. (visceral organs)

physiologic hormonal hyperplasia

endocrine hormonal stimulation (occurs in some organs)

estrogen-dependent organs

- uterus: estrogen causes hyperplasia of endometrium for implantation of zygote

- breast: develop duct work for lactation after pregnancy

pathologic hyperplasia

the abnormal proliferation of normal cells, usually in response to excessive hormonal stimulation or growth factors on target cells

- uterus: hormonal imbalance causes hyperplasia of endometrium after menopause --> cancer

- prostate: increase in testosterone will cause hyperplasia of prostate --> prostate cancer

dysplasia

abnormal changes in size/shape/organization of cells

- NOT a true adaptive change

- AKA atypical hyperplasia

- cervix, uterus, GI tract, respiratory tract are common

low/high

_____/_____ grade hyperplasia:

- how great variation is from normal

non-invasive

if changes do not penetrate the basement membrane this is known as _______ dysplasia

reversible

dysplasia may be ______ if dysplastic changes don't involve the entire thickness of the epithelium

metaplasia

reversible replacement of 1 mature cell type by another cell type

- typically associated with tissue damage/repair/regeneration

- thought that the new cell might be better suited to abrasive environment (often change is not beneficial)

- possibly due to reprogramming of stem cells

homeostasis

cellular injury happens when the cell is unable to maintain ______

- due to any factor that disrupts cellular structures or deprives the cell of oxygen and essential nutrients

reversible injury

cells can recover from injury

not lethal

irreversible injury

injury that results in cell death

reversible

these are examples of _____ injuries:

- cellular swelling (pale, increase in weight, swelling)

- fatty change (fat invades cell)

necrosis

_____ is an irreversible injury

mechanisms

general ______ of cellular injury

- ATP depletion

- influx of Ca2+ ions (causes calcification- breast cancer)

- damage from oxygen-deprived free radicals

- mitochondrial damage

- membrane damage

- DNA damage

injury

mechanisms to adapt to cellular _____:

- atrophy

- hypertrophy

- hyperplasia/dysplasia

- metaplasia

hypoxia

what is the most common cause of cellular injury?

ischemia

reduced blood supply --> decreased O2

anoxia

total lack of oxygen

- MI: acute obstruction of coronary artery with thrombus/clot

decreased

with hypoxia there is _____ ATP production (due to mitochondrial compromise), causing failure of the plasma membrane's Na/K pump and Na/Ca exchange

vacuolation

formation of large vacuoles in cytoplasm

- happens due to swelling when not resolved

apoptosis

calcium influx to the cell during hypoxia can activate enzymes which activate ______ (programmed cell death)

reperfusion

_____ injury can happen if blood flow and oxygen are restored after hypoxia

- additional injury and more harm

free radicals

have an unpaired electron (unstable)

may form chemical bonds with parts of the membrane and DNA (damaging them)

without

_____ oxygen:

- cell has hypoxic injury and becomes swollen

- with reoxygenation there is formation of free radicals which increase the risk of reperfusion injury

necrosis mechanism

injured cells swell and burst

- contents go into extracellular space and cause lots of inflammation

- MULTIPLE cells are affected

apoptosis

programmed cell death

- happens to a SINGLE cell

- phagocytes eat up cell (no inflammation)

necrosis

a bunch of cellular changes after local cell deaths

- lots of autodigestion and self lysing (rupture)

- usually results from hypoxia secondary to severe ischemic or chemical injury

coagulative necrosis

congealed/yellow areas

results from interruption in blood flow: protein denaturation --> albumin is transformed from a gelatinous, transparent state into a firm, opaque substance (infarct)

- drops pH

- organs affected most: kidneys, heart, adrenal gland

liquefactive necrosis

typically affects neurons and glial cells in brain

- brain cells are rich in digestive hydrolytic enzymes and lipids (not much CT in brain)

- tissue becomes soft and liquefied

- often triggered by a bacterial infection

caseous necrosis

commonly caused by pulmonary tuberculosis

- necrotic cells disintegrate, but debris remains

- glanulomatous inflammatory response occurs

- end result: soft granular tissue that looks like clumped cheese

- combination of coagulative and liquefactive necrosis

fat necrosis

typically found in breast and pancreas

- cellular dissolution caused by lipases

- lipases break down triglycerides, which releases FFAs. FA combine with calcium, magnesium, and sodium ions creating soaps (saponification)

- appears opaque, chalky/white area

gangrenous necrosis

large area of tissue death

- often due to blockage of blood supply

- death of tissue from severe hypoxic injury

EX: compromised circulation - lower leg - diabetic pt

dry gangrene

small amount of bacteria, brown/black dry/shriveled skin

wet gangrene

very serious

- necrotizing bacterial infection

- lots of bacteria causing liquefactive necrosis (cold, swollen, black, stinky)

gas gangrene

a type of wet gangrene

often clostridium: destroys tissue and causes bubbling gas

- progresses quickly and lethal quickly

physiologic apoptosis

average adults have 10 billion new cells and 10 billion cells destroyed daily

- embryogenesis (embryo formation)

- hormonal

- autoimmune disorder: immune cells that attack the wrong cell

pathologic apoptosis

severe cell injury (past the point of repair)

accumulation of misfolded proteins in the ER

infections/viruses

obstruction in tissue ducts/obstruction of blood flow to organs

intrinsic

______ apoptosis:

cell kills itself

extrinsic

_____ apoptosis

cell kills itself but because of signals from nearby cells

phagocytes

chemical factors are released from cells recruiting _____ to clean up debris from apoptosis

- making sure there is no inflammation