00:00 / 00:00
Acute tubular necrosis
Renal cortical necrosis
Renal papillary necrosis
IgA nephropathy (NORD)
Rapidly progressive glomerulonephritis
Focal segmental glomerulosclerosis (NORD)
Minimal change disease
Medullary cystic kidney disease
Medullary sponge kidney
Multicystic dysplastic kidney
Polycystic kidney disease
Chronic kidney disease
Renal tubular acidosis
Nephroblastoma (Wilms tumor)
Renal cell carcinoma
Renal artery stenosis
Acid-base disturbances: Pathology review
Congenital renal disorders: Pathology review
Electrolyte disturbances: Pathology review
Kidney stones: Pathology review
Nephritic syndromes: Pathology review
Nephrotic syndromes: Pathology review
Renal and urinary tract masses: Pathology review
Renal failure: Pathology review
Renal tubular acidosis: Pathology review
Renal tubular defects: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
0 / 13 complete
0 / 5 complete
20q10 deletion syndromes p. 63
acute pancreatitis and p. 406
cinacalcet causing p. 364
DiGeorge syndrome p. 644
hypermagnesemia and p. 615
hyperparathyroidism p. 344
hypoparathyroidism p. 350
pseudohypoparathyroidism p. 350
renal osteodystrophy p. 628
thymic aplasia p. 114
thyroidectomy p. 349
hypocalcemia p. 615
Now, calcium exists as an ion with a double positive charge - Ca2+ - and it’s the most abundant metal in the human body. So I know what you’re thinking - yeah, we’re all pretty much cyborgs.
Anyways, about 99% of that calcium is in our bones in the form of calcium phosphate, also called hydroxyapatite.
The last 1% is split so that the majority, about 0.99% is extracellular - which means in the blood and in the interstitial space between cells, whereas 0.01% is intracellular.
High levels of intracellular calcium causes cells to die. In fact, that’s exactly what happens during apoptosis, also known as programmed cell death. For that reason, cells end up using a ton of energy just keeping their intracellular calcium levels low.
Now, calcium gets into the cell through two types of channels, or cell doors, within the cell membrane. The first type are ligand-gated channels, which are what most cells use to let calcium in, and are primarily controlled by hormones or neurotransmitters.
The second type are voltage-gated channels, which are mostly found in muscle and nerve cells and are primarily controlled by changes in the electrical membrane potential.
So calcium flows in through these channels, and to prevent calcium levels from getting too high, cells kick excess calcium right back out with ATP-dependent calcium pumps as well as sodium calcium exchangers.
In addition, most of the intracellular calcium is stored within organelles like the mitochondria and smooth endoplasmic reticulum and is released selectively just when it's needed.
Now, the majority of the extracellular calcium, the calcium in the blood and interstitium, is split almost equally between two groups - calcium that is diffusible and calcium that is not diffusible.
Diffusible calcium is separated into two subcategories: free-ionized calcium, which is involved in all sorts of cellular processes like neuronal action potentials, contraction of skeletal, smooth, and cardiac muscle, hormone secretion, and blood coagulation, all of which are tightly regulated by enzymes and hormones.
The other category is complexed calcium, which is where the positively charged calcium is ionically linked to tiny negatively charged molecules like oxalate, which is a small anion that are normally found in our blood in small amounts. The complexed calcium forms a molecule that’s electrically neutral but unlike free-ionized calcium is not useful for cellular processes. Both of these are called diffusible because they’re small enough to diffuse across cell membranes.
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