Patho exam 1- Cellular Adaptation and Injurt

Excessive free radicals lead to

oxidative stress and cause cell death occuring

5 cellular adaptations

atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia

Hypertrophy

increase in cell size due to increased workload or stress

Hypertrophy: Physiologic example

lifting weights, runners heart

Hypertrophy: pathologic example

-cardiac enlargement d/t hypertension

-kidney enlargement d/t nephrectomy

Atrophy definition

decrease in cell size due to decreased workload, stimulation, or nutrients

Atrophy: Physiologic example

shrinking of thymus with age, immobilization (bed rest or cast)

Atrophy: Pathologic example

muscle atrophy d/t reduced use and malnutrition

Hyperplasia definition

increase in cell number due to cell proliferationn in response to hormones, growth factors, or chronic stimulation.

Hyperplasia: Physiologic example

-organ regeneration

-endometrial thickening d/t menstruation

Hyperplasia: Pathologic example

endometriosis, prostate enlargement, goiter (thyroid)

Benign Prostatic Hyperplasia defintion

Increase in number of prostate cells due to increase in cellular division

Benign Prostatic Hyperplasia patho

Testosterone causes imbalance between cellular proliferation and cellular death. Excessive proliferation causes hyperplasia where then the bladder has to work hard to push urine out causing the bladder to enlarge and weaken.

Metaplasia definition

change in cell type that has a different function; reversible

Metaplasia causes/mechanisms

adaptive response where the new cell type is better suited for the adverse environment

Metaplasia Pathologic example

change in cell type in lungs of chronic smokers

dysplasia defintion

changes in size, shape and organization of cells (same cell type but disfunctioning); reversible

dysplasia is

atypical hyperplasia, not a true adaption

Dysplasian Pathologic example

cervical/esophageal dysplasia

If hyperplasia and metaplasia are not reversed in time it leads to

cancer

What adaptions are reversible

All of them

Ischemia-reperfusion injury

Occurs when oxygen delivery is restored after an ischemic event, like a heart attack

What will reverse adaptions

removing the stressor

Ischemia

reduced blood flow to an area; causes creation of harmful substances

reperfusion

restoration of blood flow to area of deprived blood; includes harmful substance

harmful substances can cause

new damage and cell death

Hypoxia

Reduced oxygen in tissues

What is the primary mechanism for cellular injury

hypoxia

reversible cell injury

no cellular membrane damage, just swelling

irreversible cell injury

cellular membrane damage which leads to necrosis

reduction in oxygen leads to a reduction in

ATP → anareboic glycolysis -. Na/K pump reduced(3 Na out, 2 K in, requires lot of ATP) → membrane potential messed up →H20 leaks in(edema) or cellular swelling where there is organelle dysfuntion because of too much water or reduction in PRO synthesis because of the ER being dilated where ribosomes are to translate/transcribe DNA to RNA

What happens when ATP is decreased

cellular swelling, decreased protein synthesis( because of h20 in cell that messes up ribosomes on ER), decreased membrane transport, and lipogenesis which are all changes that contribute to loss of integrity of the plasma membrane. This ultimately leads to necrosis

What causes the acute cellular swelling

decreased ATP decreases Na+ pump, which causes an increase in intracellular Na+ and Ca++. Since water follows sodium, fluid will enter cell and cause it to swell

its also a early/reversible sign of cellular injury

What happens to proteins when pH is below normal

Metabolic acidosis. Proteins may misfold, triggering unfolded protein response that can ultimately lead to cell suicide

what are Free Radicals

Highly reactive molecules with unpaired electrons that cause cellular damage by stealing electrons from nearby lipids, proteins, and DNA.

Oxidative stress

when the body has too many free radicals and not enough antioxidants to neutralize them

production of free radicals can be initiated by

cell stressors such as radiation, toxins and reperfusion of oxygen

Free radicals are highly unstable molecules created when

oxygen is restored after hypoxia

what can free radicals (ROS) damage at the site of ATP synthesis

mitochondria

3 mechanisms how Free radials disrupt cellular structure or function

1. DNA modification

2. lipid peroxidation

3. Oxidative modification of proteins

DNA modification causes

results in mutations

Lipid peroxidation causes

the destruction of polyunsaturated lipids leads to membrane damage and increased permeability because it steals electrons from phospholipid

Oxidative modification of proteins causes

polypeptide chains to become fragmented and lead to protein loss, protein misfolding, and alterations in protein interaction

Necrosis

cellular death do to pathologic process of cell destruction (rupture)

Necrosis cell size

enlarged/swelling

Necrosis plasma membrane

disrupted

Necrosis inflammation

frequent and significant

Apoptosis definition

programmed cell death

Apoptosis cell size

reduced/shrinking

Apoptosis plasma membrane

intact

Apoptosis inflammation

none

Autophagy defintion

A regulated cellular process in which a cell degrades and recycles its own damaged organelles, proteins, and other components through lysosomes to provide energy and maintain survival during periods of stress, such as nutrient deprivation.

outcome of anaerobic glycolysis creates a basic or acidic cellular environment

acidic

When does Cell injury become irreversible?

Right before the point of the DNA being damaged or the cell wall membrane being damaged.

Calcium role in cellular death

Damaged to cell membrane/DNA → increased permeability →allows Ca2+ to leak into cell and mitocondria → triggers reactions such as a group of enzymes that specifically target the nucleus, DNA. cytoskeleton, membrane responsible for ceullar breakdown/ death

also if intracellular Ca 2+ increase it can inhibit muscle movements.