Patho (U1.3): Cellular Adaptation, Injury, and Death

atrophy

decrease in cell size because of decreased tissue/organ size

physiologic atrophy

normal, expected decrease in cell size due to decreased cell activity or hormones and age

pathologic atrophy

adapting due to abnormal conditions by decreasing protein synthesis and increase protein breakdown

hypertrophy

increase in existing cell counts because of increased work demands or hormonesph

physiologic hypertrophy

expected increase in existing cell counts

pathologic hypertrophy

decreasing cell counts due to abnormal conditions

hyperplasia

increase in new cell counts because of increased cellular division

compensatory hyperplasia

increase in new cell counts to allow organs to regenerate

hormonal hyperplasia

increase in new cell counts to replace lost tissue from hormonal changes

pathologic hyperplasia

increase in cell counts due to abnormal conditions such as excessive hormone or growth factor

dysplasia

atypical hyperplasia, creating abnormal changes in new cells usually located in epithelial tissues

what does dysplasia signify?

pre-disposing risk for cancer, but does NOT indicate cancer

cervical dysplasia

abnormal cells on cervix linked to HPV and detected through papsmearsm

metaplasia

reversible replacement of mature cells by less mature cells to adapt to chronic irritation and inflammationb

barret esophagus

chronic acid reflux causes lining to change to intestinal-type cells

cellular injury

damage to cells beyond their ability to adapt

3 main pathways of cellular injury

free radical formation, hypoxia/ischemia, increased intracellular calcium

what is free radical formation and how does it injure the cell

oxidation of cell structures and nuclear and mitochondrial DNA can lead to the breakdown of DNA

what is hypoxia and ischemia and how does it injure the cell

hypoxia is low oxygen and ischemia is low blood supply. this prevents the mitochondria from generating ATP which can have 3 effects:
1. sodium and potassium pump failure leading to a leaky cell
2. increased anaerobic metabolism leading to acid buildup
3. structure collapse leading to lipid buildup

how does increased intracellular calcium injure the cell

it activates enzymes that damage cells and its organelles leading to loss of ATP, DNA, and cytoskeleton

ischemia-reperfusion injury

type of ischemia cell injury (low blood supply) and are common in transplantations

ischemia phase of ischemia-reperfusion

because there is low oxygen, the body switches to anaerobic metabolism leading to low ATP, ion pump failure, and eventually cell swelling

reperfusion phase of ischemia-reperfusion injury

medical intervention or natural processes reopens blood flow but the sudden increase in oxygen leads to free radicals that can breakdown DNA and increase calcium levels

oxidative stress

caused by free radicals

pathologic calcification

abnormal calcium buildupd

dystrophic calcification

calcium deposition in dead or damaged tissues

metastatic calcification

calcium deposition in normal tissues because of hypercalcemia

apoptosis

programmed cell death of damaged or old cells to control tissue regeneration

type 1 apotosis

triggered by external signalst

type 2 apoptosis

triggered by internal stress

dysregulated apoptosis

excessive or insufficient apoptosis

autophagy

self-eating specific damaged parts of a cell as a survival mechanism

necrosis

uncontrolled death caused by cell injury and autolysis

pyknosis stage of necrosis

nucleus shrinkska

karyorrhexis stage of necrosis

nucleus and DNA fragments

karyolysis stage of necrosis

nucleus and DNA is digested

coagulative necrosis

cells are gray and firm and is common in kidneys, hearts, and adrenal glands

liquefactive necrosis

hydrolytic enzymes form cysts or pus and can be a result of inflammation or infection

caseous necrosis

cells look like cheese and is a combination of coagulative and liquefactive necrosis

fat necrosis

uncontrolled cell death in adipose tissue

gangrenous necrosis

uncontrolled cell death in bigger mass of tissues

dry gangrenous necrosis

necrosis caused by ischemia without bacterial infection

wet gangrenous necrosis

necrosis caused by bacterial infection and swelling

gas gangrenous necrosis

necrosis caused by clostridium bacterial infection

A client with pulmonary tuberculosis has an area of necrotic tissue

in the lung. The tissue appears soft, granular, and cheese-like.

Which type of necrosis does the nurse expect?

caseous necrosis

A client has severe peripheral arterial disease resulting in a

significant loss of blood supply to the foot. The affected tissue is

dry, shrunken, and dark brown to black, with no evidence of

significant bacterial infection. Which type of gangrene does the

nurse suspect?

dry gangrenous necrosis

A client has an area of damaged cardiac tissue following a

myocardial infarction. Laboratory results show a normal serum

calcium level. The nurse understands that calcium deposits in the

damaged tissue would be classified as

dystrophic calcification

A client experiences prolonged ischemia followed by

restoration of blood flow to the affected tissue.

Which cellular event occurs during the ischemic

phase?

anaerobic metabolism, decreased ATP production with failure of ion pumps

A nurse is teaching a client about dysplasia. Which statement by

the client indicates correct understanding?

dysplasia involves abnormal changes in the size, shape, and organization of mature cells

A client begins a weight-training program and develops larger

skeletal muscles over several months. The nurse recognizes this

change as which type of cellular adaptation?

physiologic hypertrophy

A client with long-standing hypertension is

diagnosed with left ventricular hypertrophy (LVH).

Which explanation should the nurse provide?

The patient has pathological hypertrophy in the cardiac muscles which is adaptation due to abnormal increased cell counts