Wk 1 CSB520 Notes

myocytes= muscle cells

Exocrine = glandular that goes into duct

endocrine = glandular that goes into blood

secretes mucous = goblet cells

Tissue types

Labile: continuously dividing

stabile: can divide when stimulated

permanent: non-dividing. If you injure them, they are irreplaceable

cardiac myocytes

skeletal myoctes

neurons

skin

GIT

reproductive

bladder

lining of exocrine ducts

liver

kidney

lung

pancreas

smooth muscle cells

endothelial cells of blood vessels (when there is inflammation

benign cells: still well-differentiated but abonrmal

Tissues need nerve innervation, blood and lymphatic supply

cell communication

autocrine (to itself)

paracinre (signal from neighbouring cells)

endocrine (into blood stream)

if cells lose these signals, they may undergo apoptosis

hypoxia = lack of oxygen

ischaemia = lack of blood supply

reperfusion: restoration of blood following period of ischaemia

Outcomes of cell stress

impaired function

mutation

death (both irreversible)

apoptosis

necrosis

adaptation

autophagy

hyperplasia: increased number of cells

metaplasia: change from one differentiated cell into another from environment change.

programmed cell death or suicide

neighbouring cells undergo necrosis

contents spill out and whole area undergoes infarct

stimulation of acute inflammation

the same stressor can stimulate either form depending on

duration

severity of application

how young/healthy the cell is

self-eating

mitochondria can be responsible for triggering cell death

phagocytosis

recognition

attachment

engulfment

killing and degradation by lysosomes

remove dodgy organelles (mitochondria), only way

way to resist and survive stressful situations

some cells are more resistant to stress

young cells choose to shrink to need less oxygen and nutrients

can come back to original size

in older people, autophagy is inhibited and cell will undergo apoptosis

loss/reduced tissue function

only ever pathological

physiological or pathological

active dismantling of cell

form apoptotic bodies (membrane bound)

no inflammation or scarring

one cell can die without impacting others

Physiological: embryonic development, tissue homeostasis, removal of redundant cells, immune function

pathological: pathological atrophy to stop necrosis, transplant rejections, auto-immune diseases, infections

is an active proces

is a passive process

Atrophy

combination of autophagy and apoptosis

decreased cell size

decreased cell number

reversible? depends on type of cell. If the cell can divide it can.

cells that have shrunk can get bigger

ones that can't divide can't be replaced

Lesser degree of stress is needed to start necrosis

sudden severe stress is always necrosis no matter how healthy the cell is

decrease in cell size

opposite of hyperplasia and hypertrophy

hyperptrophy: no cell division, but cells get larger

take away the stress, the adaptation is reversible

all active processes

involution: tissue returns to normal size from reduced hormone levels

increased workload on left ventricle: sustained increase in HR or force of contraction

caused by over-activation of SNS, valve disease, hypertension

right: heart defect, increased pressure in pulmonary circuit from congestion, loss of vasculature

reduces reserve capacity of heart so more likely to fail