INTERNATIONAL MEDICAL SCHOOL

BACHELOR OF MEDICAL SCIENCES

(BMS)
GENITOURINARY SYSTEM - QAP20902T
ASSIGNMENT 1

NAME : ILHAASHINI A/P KRISHNAN

ID : 012021090323
LECTURER : DR MUSTAFA FADILMOHAMMED
SUBMISSION : 14TH MARCH 2022
Renal functions
The renal system, also known as the urinary system, is a group of organs in the body that
work together to filter metabolic wastes and foreign substances such as urea and uric acid,
creatinine, and excess fluid and ions such as sodium and potassium from the kidneys, as
well as eliminate other waste products such as water from the bloodstream through urine.
The regulation of blood pH, which has a normal value of 7.4, is another function of the renal
system. In addition, the kidney controls the acid-base balance. The renal system is also
involved in the regulation of body fluid, which is the plasma osmolarity. The antidiuretic
hormone detects plasma osmolarity, which is the concentration of solutes such as sodium,
potassium, and glucose in the plasma with a normal value of 300 mOsm/lt .
The main renal function is excretion of Metabolic Waste and Foreign Substances .End
products of metabolic activities are constantly formed in our bodies. In most situations, the
end products are hazardous at high quantities and are of no benefit to the body. As a result,
they must be excreted at a rate equal to their production. Urea (from protein), uric acid (from
nucleic acids), creatinine (from muscle creatine), urobilin (a haemoglobin breakdown end
result that gives urine its colour), and hormone metabolites are some of these products.
Foreign substances, including many commonly prescribed medications, are also eliminated
via the kidneys. In many circumstances, the kidneys and the liver work together. Many
organic compounds are metabolised by the liver into water-soluble forms that are easier for
the kidneys to process.
Regulation of Water and Electrolyte Balance also one of the renal functions.Water, salt, and
other electrolytes enter our systems at varying rates, causing changes in the amount and
concentration of those substances. To maintain optimum levels in the body, the kidneys vary
their excretion of electrolytes and water. They achieve this by maintaining balance, or
matching output to input in order to maintain a consistent amount in the body. Consider
water balance as an example. Our water intake is irregular, and it is only seldom driven by
body needs. We drink water because we're thirsty, but we also drink it because it's in drinks
we drink for reasons other than hydration. Furthermore, solid meal generally contains a lot of
water. Increases in water content cause the kidneys to increase the outflow of water in the
urine, returning body water to normal levels. The same rules apply to a wide range of
electrolytes and other compounds with varying inputs.
The peptide hormone erythropoietin stimulates the synthesis of red blood cells in the bone
marrow. The liver produces erythropoietin throughout embryonic development, whereas the
kidneys are the main source in adults. It is secreted by a specific type of interstitial cell found
in the cortical interstitium along the border between the renal cortex and the medulla. A
decrease in the partial pressure of oxygen in the secreting cells' local environment triggers
its secretion. Although renal blood flow is high, renal metabolism is also high, and local
oxygenation falls in anaemia, which can be caused by blood loss, arterial hypoxia, or
insufficient renal blood flow. All of these factors increase erythropoietin secretion. However
in chronic renal failure, renal metabolism falls, resulting in lower oxygen consumption and
therefore higher local tissue oxygenation. This “fools” the erythropoietin-secreting cells into
diminished erythropoietin secretion. The ensuing decrease in bone marrow activity is one
important causal factor of anemia associated with chronic renal disease.
Other renal function is Gluconeogenesis.Whether we've just eaten sugary doughnuts or
gone a week without meals, our central nervous system is a compulsive user of blood
glucose. When carbohydrate consumption is reduced for more than half a day, our bodies
begin to generate additional glucose from noncarbohydrate sources (gluconeogenesis)
(amino acids from protein and glycerol from triglycerides). The liver is responsible for the
majority of gluconeogenesis, but the kidneys also play a role, especially during a prolonged
fast.
Regulation of Vitamin D production is also one of the renal function.When we think of vitamin
D, we usually associate it with sunlight or milk additions. Vitamin D is synthesised in the
body by a sequence of metabolic changes, the last of which takes place in the kidneys.
Calcitriol, the active form of vitamin D (1,25-dihydroxyvitamin D), is produced in the kidneys,
and its rate of synthesis is controlled by hormones that govern calcium and phosphate
balance as well as bone health.
Regulation of Vascular Resistance,Aside from supplying enough volume for the
cardiovascular system, the kidneys also play a key role in the generation of vasoactive
chemicals (via the renin-angiotensin-aldosterone system) that regulate vascular smooth
muscle. As a result, peripheral vascular resistance and, as a result, systemic arterial blood
pressure are affected. Hypertension is caused by pathology in this component of renal
function.

Glomerular filtration rate (GFR) and the methods that estimate GFR.

The flow rate of filtered fluid through the kidney is described by the glomerular filtration rate (GFR),
which is one of the indicators of kidney function. It is the total amount of plasma filtered by both
kidneys. It also represents the flow of plasma into the Bowman's capsule from the glomerulus over
time. Blood enters individual glomerular tufts via the afferent arteriole and exits by the efferent
arteriole, giving the kidneys around 20% to 25% of cardiac output. Through the renal blood
flow(RBF), only plasma can pass through the structures including the glomerulus . As a result, the
renal plasma flow (RPF) is a more specific expressions.
The RPF is about 600 to 720 ml per minute. Because organic and inorganic solutes can only
be found in the ultrafiltrate, which is the fluid in the Bowman's capsule, they are freely
filtered, and plasma is maintained at the same concentration. The GFR is around 120 ml per
minute, or 180 litres per day. On the other hand, the average daily urine output is only 1.5
litres. A cultured tubular network is required for the reabsorption of 178.5 L. Fluids travel
across the glomerular capillary in response to the hydrostatic pressure from the afferent
arterioles, resulting in glomerular filtration. Firstly, the blood from the body system enters the
glomerular capillary through the afferent arterioles into the kidneys. Then, the glomerular
filtration acts and filters out the renal corpuscle which is the filtration unit of the vertebrate
nephrons. After filtration, the large proteins which are the plasma proteins and cells which
are left unfiltered stays behind and therefore filtered into nephrons.
The glomerular filtrate is a fluid that has been filtered from the capillaries of the glomerulus
and is found in the lumen of the Bowman's capsule of the nephron. It has the same plasma
composition as plasma, but none of the bigger components, such as plasma, are present.
Fenestrated endothelium cells, podocytes (also known as glomerular visceral epithelium
cells), and the glomerular basement membrane are the three filtration membranes found in
the glomerulus. The glomerular filtration barrier is made up of these three components. The
glomerular basement membrane is covered by the glomerular epithelium or podocytes,
which in turn is covered by the fenestrated endothelium. The podocytes' job is to surround
the capillaries with cellular extensions known as foot processes. It has foot-like extensions,
commonly known as pedicels, with filtration slits between them. Both the glomerular
capillaries and Bowman's capsule serve as blood filters.The filtration found in Glomerular's
space called Glomerular filtrate.
The glomerular capillaries are fenestrated, indicating there are transparent regions between
the endothelial cells, and there are large pores between the endothelial cells. Because,
unlike systemic capillaries, which take blood from high-resistance arterioles and drain to low-
resistance venules in a gradient system, glomerular capillaries are connected to high-
resistance arterioles on both ends (afferent and efferent arterioles). The filtration coefficient
(Kf) and the rate of glomerular filtration increase as permeability increases. It's also small
enough to keep all red blood cells, platelets, and white blood cells from going through, and
the holes are lined with negative charges to prevent blood proteins from filtering. All filtrates
that can pass through the membranes, such as water, tiny molecules, and ions, enter the
renal tubules and must pass via the glomerular filtration slits created in between the pedicels
of the podocytes.
The molecular weight and charge of the molecules are the two factors that determine
glomerular filterability. The renal blood flow rate is approximately 1200 mL/min, the renal
plasma flow rate, which is the fraction of plasma in the blood, is approximately 650 mL/min,
the filtration fraction, which is the plasma that is filtered into the lumen of the Bowman's
capsules, carries an average of 20%, the amount of filtrate produced each minute of the
glomerular filtration rate (GFR) is approximately 125 mL/min, which is also equivalent to 180
L/day.
The GFR is determined by a number of parameters, including the filter thickness, surface
area, colloidal osmotic pressure of the glomerulus, magnitude of any forces favouring
filtration, and magnitude of any forces opposing filtration. It is further influenced by two
additional factors: the filtration coefficient (Kf) and the net filtration pressure (NFP). The
higher the glomerular filtration rate, the higher the filtration coefficient, and vice versa. The
net filtration pressure(NFP) is also the same . The GFR is determined by the sum of the
hydrostatic pressure, colloid osmotic forces across the glomerular membrane, Bowman’s
capsule hydrostatic pressure which can be caused by the ureteral stones and obstruction of
the urinary tract, and the glomerular capillary filtration coefficient.
The decreased GFR is caused by the constricted afferent arteriole.When the efferent
arteriole is dilated, the GFR drops as well. The constricted efferent arteriole causes the
higher GFR. The dilated afferent arterioles also contribute to the rise. Measurement of
plasma creatinine, which has a normal value of 1 mg/dl, measurement of blood urea
nitrogen, which has a normal reading of 15 mg/dl, and the inulin clearance and creatinine
clearance tests are also used to indicate the increase and decrease of GFR.
ACUTE TUBULAR NECROSIS
Abrupt tubular necrosis (ATN) is a kidney condition in which the tubule cells of the kidneys
are damaged, leading to acute kidney failure. This illness causes a shortage of oxygen and
blood flow to the kidneys, causing them to be damaged. A sudden and prolonged decrease
in glomerular filtration rate (GFR) between minutes to days after an ischemia or nephrotoxic
shock is also known as nephropathy. After a hypotensive or hypovolemic episode, or toxic
damage from rhabdomyolysis or the administration of a nephrotoxic medication, this causes
an abrupt rise in urea and creatinine.
Furthermore, the rise in intratubular pressure caused by inflammation lowers the glomerular
filtration rate. Because of the tubular backleak, the rate of tubular fluid flow will be lowered,
resulting in a lower glomerular filtration rate. This results in oliguria or hypouresis, which is a
decrease in urine flow. When there is fewer than 400 millilitres of urine per day, this is
measured. The particular amount for newborns and children is determined by their weight
(less than 1 millimetre per kilogramme per hour for infants and less than 0.5 millimetres per
kilogramme per hour for children). Acute tubular necrosis is divided into three stages. The
first phase is the onset or initiating phase, the second phase is the maintenance phase and
the third phase is the recovery phase.
Pre-existing chronic kidney illness, cardiovascular disease, extracellular fluid volume
depletion, and numerous renal shocks are all risk factors for acute tubular necrosis.
Hyperkalemia, or a high potassium level, metabolic acidosis, decreased calcium, elevated
phosphate, and hypoalbuminemia are all consequences of this condition. The tubules in the
kidneys are responsible for filtering waste materials and fluid. This condition d ue to renin-
angiotensin vasoconstriction, the glomerular filtration rate is affected. Prostaglandin and
nitric oxide levels drop in endothelin.
This condition is caused by a lack of blood flow and oxygen to the kidney tissues (ischemia
of the kidneys), or it might be caused by a poisonous or harmful substance damaging the
kidney cells. Exogenous and endogenous toxins are the two types of toxins that exist.
Antibiotics including aminoglycosides, cephalosporins, and amphotericin B are examples of
exogenous toxins. Furthermore, antiviral medications, antineoplastics such as cisplatin and
methotrexate, and contrast media used in radiographic imaging through IV contrast could
damage the tubule ring, resulting in contrast-induced nephropathy and vasoconstriction.
Tubular damage can also be caused by heavy metals and ethylene glycol. Exogenous toxins
include bacterial endotoxins, which are released when a person has a bacterial infection,
and myoglobin from rhabdomyolysis, which can be released into the bloodstream and harm
the kidneys and renal tubules if a person suffers a significant injury to their skeletal muscles.
Acute tubular necrosis can also be caused by haemoglobin damage to the renal tubules.
Acute tubular necrosis is another common cause of kidney failure in hospitalised patients.
The risks of contracting this disease include muscle injury or trauma, recent major surgery,
blood transfusion reaction, septic shock, and hypotension, which causes low blood pressure
and volume to the kidneys for more than 30 minutes, resulting in ischemia.
Ischemic damage of the renal tubules can be induced by a decrease in blood circulation
volume caused by bleeding, fluid losses from the skin and gastrointestinal tract, and the
renal system. A person's risk of developing ATN may also be increased if they have
diabetes-related liver disease or renal damage. People who also use kidney-toxic
medications such as aminoglycoside antibiotics and amphotericin, an antifungal agent. A
little amount of urine output, edoema and fluid retention, nausea and vomiting, difficulty
waking up or lethargy, feeling sluggish, and disorientation are all indications of acute tubular
necrosis.

References

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