This topic covers the concept of Calcification. In this, I cover both well known types of calcification, including dystrophic and metastatic calcifications, and also talk about calcium related pathologies such as Gamma-Gandy Bodies, Psammoma Bodies, Hypercalcemia, and Calcification related conditions such as Calcific Aortic Stenosis, Heterotrophic Ossification, Calcinosis Cutis, Monckeberg’s arteriosclerosis among others. Hope you guys enjoy! Continue reading Calcification
This topic covers the mechanism of irreversible cell injury. We talk about each mechanism in which cells can be irreversibly damaged, including ATP depletion, Mitochondrial Damage, Influx of Ca2+ and disruption of Ca2+ homeostasis, Reactive Oxygen Species, Membrane Damage, DNA and Protein Damage. Continue reading Mechanism of Irreversible Cell Injury
This is the second post in the series: Pathologic Cell Injury and Cell Death. This topic, Necrosis, involves cell death that is done unintentionally by the cell. I will talk about all the different mechanisms of necrosis, pyknosis and its variants, and the different morphological types of necrosis, including Coagulation, Liquefactive, Fat, Caseous, Fibrinoid, Gangrenous and Avascular. Continue reading Pathologic Cell Injury and Cell Death II – Necrosis
This topic is Part 1 of a 4 Part Series. The first topic, Reversible Cell Injury, covers the physiology and pathology of reversible cell injuries, and what happens to a cell when a cell is unable to adapt to the stresses of the environment. I will discuss histological changes in cells, Cellular Swelling and Steatosis. Continue reading Pathologic Cell Injury and Cell Death I – Mechanism of Reversible Cell Injuries
This topic covers the concept of Autophagy in detail, a concept I’ve covered briefly in “Waste Disposal In Cells” and “Cellular Adaptation To Stress.” I have explored the topic in full detail here, including the classes, types, and importance, and as usual , included several diagrams, videos and questions. I hope you find this useful! Continue reading Autophagy
Waste Disposal In Cells
I just put my garbage out, the useless stuff I didn’t need anymore. Right after that I thought, Wait.. how do cells get rid of all the things they make? Turns out there is indeed a way for cells to do that – literally put out the garbage. All our cells are like little humans aren’t they? Living their own little life. And that’s what brings us to today’s topic – Waste Disposal In Cells.
Waste disposal in cells is done through 2 pathways:
Lysosomes are membrane bound organelles containing more than 40 different enzymes.
These enzymes include proteases (break down protein), lipases (break down lipids), nucleases (break down nucleotides of nucleic acids), glycosidases (break down glycosidic bonds in complex sugars), phosphatases (break down phosphate bonds) and sulfatases (break down sulphate bonds), just to name a few. Look at the diagram below to see a few other classes of enzymes present in lysosomes.
It is clear that lysosomes are very equipped to break down almost anything the cell needs to get rid of. Obviously, these enzymes must be kept separated from the rest of the cytoplasm, and this is done by the single layer of membrane. If the membrane is ruptured, the enzymes will escape and destroy the cell from the inside out! It would be like the plot of The Dark Knight Rises, where Bane releases all the prisoners (enzymes) of Blackgate Penitentiary (single layer of membrane), who then proceeded to destroy the city.
Lysosomal enzymes function best at an acidic pH of less than 5. Thus, all the lysosomal enzymes are collectively referred to as acid hydrolases. The fact that the enzymes function best at an acidic pH is actually a protective mechanism, in addition to the single layer of membrane. This is because if the enzymes to manage to escape the lysosome, they will be far less active at the higher pH of approximately 7.3, in the cytosol.
This pH of
Lysosomal enzymes are all originally synthesized in a structure within the cell known as the rough endoplasmic reticulum, alongside all other proteins. However, how do the enzymes become lysosomal enzymes?
Cellular Adaption To Stress
Cellular adaptation refer to (usually) reversible changes in size, number, phenotype or appearance, metabolic activity or functions of cells in response to adverse environmental conditions or internal bodily stresses.
Basically, just as we react to something in our environment, cells don’t just sit there and take their punishment – they change to try to conquer the problem.
There are 4 important ways in which they do this:
Hypertrophy and Hyperplasia
Hypertrophy is a cellular response that involves the increased size of cells, that results in an increase in size of the affected organ.
Note that there is no increase in the number of cells, rather JUST the size. This type of cellular adaptation to stress occurs in a number of different cells, and is usually coupled with another type of cellular adaptation, hyperplasia.
Hyperplasia is a cellular response that involves the increase in number of cells in response to a stimulus.
Both hyperplasia and hypertrophy occur as compensatory mechanisms to an increased workload on the organ or cell.
To remember which is which, think of the prefix and suffix that make up the word. The suffix “plasia” means “development” and thus hyperplasia means “increased development,” corresponding to an increase in the number of cells. Similarly, “-trophy” means “sustenance, nutrition” and thus, hypertrophy refers, in fact to the very mechanism of hypertrophy, an increase in factors that sustain and allow growth of the cells, which will be explained later.
If cells are divided into cells that are capable of dividing, and cells that are incapable of dividing, we can also divide the way they react to increased stress.
- Cells capable of dividing respond to an increased workload using both hyperplasia and hypertrophy.
- Cells incapable of dividing can only respond to an increased workload by hypertrophy. An example of this is in myocytes, or cardiac muscle cells in myocardial fibres. Thus, the heart mainly responds to an increased workload by hypertrophy. Other examples are adult skeletal muscles and neurons.
Physiologic vs Pathologic Hypertrophy and Hyperplasia:
Hypertrophy and hyperplasia, while it can be physiological to aid the body, may also be disease related, or pathological, and is a very important indicator of disease.
Physiologic Hypertrophy: is caused by an increased workload, increased functional demand or stimulation by hormones and growth factors. Of these, the most common stimulus for hypertrophy is increased workload. An example of workload induced hypertrophy would be the muscle enlargement in bodybuilders as muscles are forced to tolerate new loads. An example of hormone-induced hypertrophy is within the endometrium and myometrium of the uterus, as estrogen upregulation during the follicular stage of the menstrual cycle stimulates an increase in muscle proteins in the stroma of the endometrium and the large smooth muscle layer of the myometrium, and thus, muscle size.