Now that we're done talking about poo, let's talk about pee! There's not too much you need to know about this for this unit though, which is why this is going to be the only post about it for a while.
Just in case you don't remember anything about renal function:
Describe some of the factors that could promote a urinary tract infection (UTI)
Urinary tract infections are more common in women due to the proximity of the anus and urethra. Other risk factors for UTIs include uncontrolled diabetes, as high glucose levels "feed" the bacteria lurking down there, and anything that might obstruct the flow of urine (such as kidney stones).
Distinguish between cystitis and pyelonephritis. Describe their symptoms. What are cell casts?
Cystitis is infection of the bladder, whereas pyelonephritis is infection of the kidneys themselves. Pyelonephritis is a lot rarer, and usually arises from a pathogen ascending up the ureters, but sometimes the pathogen may be blood-borne. Cystitis and pyelonephritis are both types of UTIs and share many of the same symptoms, such as dysuria (painful urination), urgency, bacteriuria (bacteria in the urine), haematuria (blood in the urine) and other systemic signs such as fever and leukocytosis.
There are, however, a couple of symptoms that are unique to pyelonephritis. One of these is flank pain, or pain in the area of the kidney. Another symptom is cell casts. Cell casts occur when inflammation increases the leakiness of the blood vessels, causing protein to leak into the urine. Protein in the urine causes the formation of jelly-like "casts" which may also contain cells.
How does "strep throat" lead to glomerulonephritis?
Streptococci are pretty nasty. I've already mentioned before how untreated streptococcal infections can lead to rheumatic fever and rheumatic heart disease. Unfortunately, their ability to cause pain and suffering doesn't end there- they are also the most common cause of glomerulonephritis, or inflammation of the glomeruli! (Read here if you don't remember what glomeruli are.)
Just like with rheumatic fever, acute poststreptococcal glomerulonephritis (APSGN) develops around two weeks after a streptococcus infection, such as strep throat. It occurs due to antibody-streptococcus complexes lodging in the small glomerular capillaries. This activates complement, a key molecule in the immune system, as described several times before. This, in turn, leads to inflammation, increased permeability of the glomerular vessels, leakage of protein and red blood cells into the filtrate, and, if severe, a decrease in GFR as the kidneys overcompensate for the dilated blood vessels by inducing vasoconstriction.
Describe the symptoms of APSGN. How does altered renal function account for these symptoms?
Signs and symptoms include flank pain (like in pyelonephritis), the presence of protein, blood or red blood cell casts in the urine (leading to "smoky"-coloured urine) and facial oedema due to the reduction of plasma proteins which would normally assist in holding fluid in the blood. Just like with rheumatic fever, there may be an increase in antibodies against streptococcus infection, such as ASO (antistreptolysin O) and ASK.
In severe cases of APSGN, there may be vascular congestion, due to all of those antibody-strep complexes clogging up the blood vessels. This causes an increase in serum urea (which can be measured via BUN- blood urea nitrogen) and creatinine, which would normally be eliminated via the urine. On the other hand, there is a decrease in serum complement, as that's all down in the kidneys fighting the infection. Acidosis, due to reduced elimination of acidic compounds, and oliguria (reduced production of urine) also result due to congestion. At the same time, the reduced blood flow through the kidney is detected by nephrons in the juxtaglomerular apparatus, which produce renin and kick off the RAAS pathway, which ultimately results in an increase in blood pressure- not what you want when you have vascular congestion!
Treatment of APSGN, aside from trying to treat the strep infection early, is mainly symptomatic. Sodium, fluid and protein have to be restricted, as these are no longer being eliminated as efficiently as before. Glucocorticoids may be needed to keep inflammation down, and antihypertensives may be required to counteract the increased blood pressure from RAAS activation.
Describe the two most common types of renal stones, their source and their solubility in acids or bases.
Renal stones are also known as kidney stones, nephrolithiasis or urolithiasis. They form around tubular debris, which is basically debris from broken down luminal epithelial cells in the nephron. Their main causes are excessive amounts of insoluble salts and insufficient fluid intake.
The most common types of stones are calcium salts. One of these is calcium oxalate. Usually dietary calcium keeps oxalate in the stool, but in the case of diseases such as IBD, where fat absorption is impaired, calcium might bind to the fat instead, allowing oxalate to become taken up by the body. Another common calcium salt is phosphate, which is less soluble in alkaline (basic) urine, presumably because less phosphate will be ionised at basic pH.
Another common type of stone is derived from uric acid. Uric acid stones may result from gout, which is a problem with purine metabolism, or from cancer chemotherapy. In contrast to calcium phosphate stones, uric acid stones are less soluble in acidic environments, presumably because less uric acid will be ionised at acidic pH (uric acid will hold onto its protons more readily than the stuff in the environment around it).
Describe the signs and common treatments of renal stones.
As you probably know, kidney stones come with a lot of pain. Specifically, this pain is flank pain, and is colicky (comes and goes with the contractions of the ureters). Treatments generally involve getting rid of the stones by lithotripsy (using shockwaves to break up the stone) etc. Increasing the fluid intake can also help. Potassium citrate can also help treat kidney stones, as the citrate can more reaily bind to calcium, allowing the more soluble calcium citrate to be washed out of the kidney. Changing urine pH to make the stone more or less soluble (so acidifying the urine in the case of a calcium phosphate stone or alkalising it in the case of a uric acid stone) is another possible solution.
Give examples of potential causes of acute renal failure. What are the two most common conditions leading to chronic renal failure?
Renal failure is essentially when the kidneys stop working. Acute causes include glomerulonephritis, circulatory shock (not enough blood getting to the kidneys), burns (broken down red blood cells clog up the vessels) and nephrotoxins such as excessive amounts of NSAIDs (inhibit prostaglandins, which usually cause vasodilation). The most common chronic conditions that cause renal failure are diabetes and hypertension.
Describe the symptoms and principles of treatment of end stage renal failure.
To talk about end stage renal failure, I'm first going to talk about what the different stages are.
In the first stage, there is a decreased reserve. Normally, we have many more nephrons than we actually need. If some of these fail, the others can compensate, but that means that you still have an overall reduction in the number of working nephrons.
In the second stage, renal insufficiency, so many nephrons have stopped working that the kidney isn't quite keeping up with everything that it needs to do. This causes a decrease in GFR (glomerular filtration rate), which in turn leads to increased serum creatinine and urea. The increased urea (as measured by blood urea nitrogen, as mentioned earlier) can affect neurons, including those that control appetite, so anorexia (loss of appetite) is another symptom that may occur. The decrease in GFR also causes an increase in renin production, activating the RAAS pathway and causing an increase in blood pressure. Although many nephrons aren't working, the nephrons that are working have a limited ability to reabsorb fluids, so polyuria (excess urine production) is another symptom. Finally, erythropoietin (EPO) and vitamin D3, which are normally either produced or activated by the kidneys, cease to do their job, so anaemia and/or osteoporosis may result.
Finally, we reach the end stage of renal failure, where there's hardly any working nephrons. Symptoms include oliguria (reduced urine production), hyperkalemia (high potassium), hypocalcemia, acidosis and azotemia (increased levels of nitrogen-containing compounds, such as urea- high urea can be specifically referred to as uremia) due to the kidneys not being able to get rid of or reabsorb the stuff that it needs to.
Treatment for end stage renal failure is, unfortunately, not curative. The first step is to control the diet by making sure not to take in too much of the stuff that your body can no longer get rid of effectively, for example phosphate, protein and fluid. Medications can be taken to help with anaemia (such as injectable EPO) and hypertension. Transplants may also be considered, though this is no permanent solution: most transplanted kidneys only last around 10 years or so before the immune system destroys it.
Many patients may have to undergo dialysis, which is where the blood is removed, filtered through a machine and then returned to the body. There are two main types of dialysis. In haemodialysis, patients have to come to the hospital several times a week for hours at a time. Blood is removed from their arm, filtered through a machine and returned. Peritoneal dialysis, which can be done overnight at home, fills the peritoneal cavity with dialysate (fluid used for dialysis), which is drained by another tube. The dialysate in both cases contains several osmotically active particles so as not to cause too much fluid to move into the body via osmosis. The fluid always contains glucose so that the body can maintain its supply of glucose.
And that's all you need to know about kidneys. Yay!
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