Lecture 1: Altered Cellular Biology JG~MM Flashcards
(55 cards)
Normal Homeostasis
Normal internal equilibrium
Stress (Insult)
Stimulus which upsets normal homeostasis
Compensation
The body’s attempt to maintain normal homeostasis under stress
Cell Injury
Result of a stimulus in excess of a cell’s immediate adaptive response
Reversible Cell Injury
Injury which does not kill the cell (anything that doesn’t kill me makes me stronger)
Works at the cellular level but NOT at the tissue level
Irreversible Cell Injury/Cell Death
Injury that results in cell death
Apoptosis
Clean controlled cell death
Necrosis
Messy uncontrolled cell death
Cell Adaptation
Adaptation (compensation) that occurs at cellular level
Atrophy
● ↓ in the size of cells
● “a”- without, “trophy”- feast (now statuette)
● No feast: looks like cells are starving
Hypertrophy
● ↑ the size of the cells ● Lots of feasting, much bigger ● Fat cells (adipocytes) ● Skeletal muscle cells ● Cardiac → hypertrophy
Hyperplasia
● ↑ in number of cells
● “Plasia” (e.g. plastic) = form
● Hyperplasia: most everything else
○ I.e. benign prostatic hyperplasia
Metaplasia
● Change from one cell type to another cell type
○ Can be normal or abnormal
● I.e. columnar → stratified squamous → in bronchioles of smokers
○ Result of a stressor
○ GERD: esophageal lining is stratified squamous
then turns to columnar
○ Smoking: ciliated pseudostratified → stratified
squamous
■ If quit smoking goes back to what should be?
● Metaplastic tissue can become dysplastic
*chronic injury or irritation
Dysplasia
● Abnormal cells that are not necessarily cancer
● “dys” = bad/painful + form
● Cells that are not a legitimate cell type
● NOT necessarily cancerous, but precancerous (could progress to cancer)
○ In reality almost ANY cell in body can progress
to cancer
○ But dysplastic cells are well on the way to
becoming cancer
● NOTE: cancer cells will almost always be dysplastic
*Persistent severe injury or irritation
Neoplasia
● Abnormal disorganized new growth, sometimes referred to tumor (swelling that is abnormal)
● Not all neoplasia is cancer, but all cancer results in neoplasia
○ I.e. Warts: not cancer but neoplasia. (Warts are also dysplasia)
Hypertrophy in Cardiac Muscle
● Caused mainly by hypertension, aortic stenosis (valve doesn’t open all the way)
○ No rest for the heart during these conditions as compared to exercise
● Power athletes (i.e. cyclists, rowers, sprinters) usually show cardiac (left ventricular) hypertrophy but not as much as pathological hypertrophy
○ Left ventricular hypertrophy in an athlete is not usually a problem
● Stressor that injures a cell but doesn’t kill it
○ Moving heavy boxes, injures cells & they start adapting, but sore next day (DOMS)
○ When you move again within a week you don’t feel so bad
○ Heart attack: if cells don’t die they prepare for future heart attack
○ Dead cardiomyocytes however are not replaced by new myocytes
Myocardial cells ONLY undergo hyperplasia or hypertrophy?
hypertrophy
What do skeletal muscle, cardiac muscle, and neurons all have in common?
Do not undergo hyperplasia.
ATP depletion
● O2 deficiency greatly ↓ ATP production
● Blood flow ↓ → don’t get enough O2 → without O2 don’t get enough ATP production
● Lack of ATP prevents Na+/K+ ATPase
○ Na+ flows in → H2O follows in → cell swells
Free Radicals & Reactive O2 Species (ROS)
● Cause oxidation of membranes & other structures
○ I.e. hydrogen peroxide on skin: bubbles & skin bleached & burn
● Particularly problematic with reperfusion
○ Restoring blood flow to area can cause oxidative damage (unpaired electron)
*see slide 8 drawn graph for athlete vs non-athlete
↑ Intracellular Ca2+
● Low ATP & Na+ gradient prevent removal of Ca2+
● Release of Ca2+ from mitochondria & ER
● Ca2+ activates many enzymes & apoptosis
● Very high levels Ca2+ signals apoptosis
● A lot of Ca2+ causes cell death
Defects in Plasma Membrane
● Loss of Na+ gradient, activation of proteases & phospholipases
● Permeable plasma membrane prevents normal cell function
● Lose normal cell function
Ischemia (slides 9 & 10)
● Tissue not getting new O2 → becoming hypoxic → with ↓ in ATP production (from 34 ATP → to 2 ATP)
● Glycolysis ↑ to get as much ATP as possible
○ This also creates H+ & cells & tissue become acidic (acidosis)
● Lactate is pyruvate that has H+ added; lactate buffers H+
● Tissue becomes acidic, pH falls, nucleus begins clumping (not irreversible) but can’t access DNA
○ No O2 to neutralize the H+ in tissue
● ↓ in pumping Na+ out, lose gradient, H2O follows, ↑ extracellular K+ (from K+ leak channels) d/t no ATP
○ Lose electrical gradient
○ Resting membrane potential begins to go up & start depolarizing cells
● Ca2+ continues to come into cell & is unable to be pumped out
○ Needs contraction but unable to d/t no ATP
● Acute swelling of cell d/t H2O coming in
● Dilation of Rough ER
○ Ribosomes begin to detach, ↓ in protein synthesis (to save ATP), lose ability to maintain cytoskeleton (not making actin d/t ↓ in protein synthesis)
● Now membrane damage begins to take place
● Loss of membrane allows things to leak out:
○ Lactate dehydrogenase (LDH), creatine-kinase (CK): indicators that cells somewhere in body are dying
● Lysosomes swell
○ When they rupture, lysosomes release digestive enzymes that begin breaking the cell down (autolysis)
● Irreversible Injury
○ Defects in the membrane
○ Karyolysis
■ DNA is chopped up & game over (not able to reproduce)
Karyolysis
dissolution of a cell nucleus
