·
Tf/P ratio = 1 means substance is freely
filtered.
If less than 1,
substance is not freely filtered.
·
In ACIDOSIS: K+
filtration: increase, Serum K+: decrease, K+excretion: increases
·
·
The H+ produced is buffered mainly by the large amount of
hemoglobin in the red blood cells. Bicarbonate is not an effective
buffer of volatile acid.(CO2).
·
The major structural differences between epithelial cells of
the proximal and distal tubules account for the fact that 65% of
glomerular filtrate is reabsorbed in the proximal tubule and that the proximal
tubule is more permeable to water.
The proximal tubule has an extensive brush border
composed of numerous microvilli, which markedly increase the surface area for
reabsorption, and the tubule also has an extensive network of intracellular
channels.
The distal tubule has many more tight junctions
between cells, which makes it less permeable to water. No significant
difference in basement membrane thickness is observed between the proximal and
distal tubules.
·
The macula densa senses the chloride concentration
of the fluid flowing from the ascending limb of Henle's loop into the distal
convoluted tubule.
An increase in NaCl concentration occurs when the
amount of fluid flowing through the ascending limb increases because there is
less time available for the reabsorption of NaCl. The resulting increase in Cl–
concentration results in the release of adenosine from the macula densa.
Adenosine constricts the afferent arteriole resulting
in a decrease in filtration and a return of the flow rate within the nephron
toward normal. This response is referred to as tubuloglomerular
feedback.
·
Persistent diarrhea will result in a metabolic acidosis,
due to the loss of the bicarbonate-rich secretions from the pancreas and
gallbladder. The ensuing metabolic acidosis will decrease the plasma
concentration of HCO3–, decreasing the amount of bicarbonate that is filtered
into the proximal tubule. At the same time, the metabolic acidosis will
increase ammonia production by the proximal tubule as well as H+ secretion and
production of new bicarbonate by the distal nephron. Because the metabolic
acidosis is produced by the loss of bicarbonate, the anion gap will remain
within normal limits.
·
The movement of K+ into cells is facilitated by the presence
of insulin and epinephrine. During exercise, epinephrine hastens the
movement of K+ into muscle cells, preventing the accumulation of K+ in the
extracellular space around active muscle cells.
·
Free water clearance is the amount of water
excreted in excess of that required to make the urine isotonic to plasma. It is
calculated using the formula
CH2O = V × [1 – (UNa + UK)/PNa]
Free water clearance is positive when the urine is
dilute (more than a sufficient amount of water is excreted), and free water
clearance is negative when the urine is concentrated (not enough water is
excreted to make the urine isotonic to plasma).
·
Phosphate transporter is electrically neutral,
requiring 2 Na+ molecules for every HPO42– molecule that it transports. The
transporter is inhibited by parathyroid hormone (PTH).
·
Alkalosis
dissociates protein molecules, which bind ionised calcium. The
hypocalcaemia opens Na+ - channels, and the influx increases the excitability
of neuromuscular tissues, which releases tetanic cramps.
·
Primary
hyperaldosteronism (Conn’s hypercorticism disease) and all types of
secondary hyperaldosteronism also lead to hypernatraemia combined with
hypokalaemia and enlarged blood volume. Cerebral failure and convulsions are
alarming signs, but there are no specific symptoms and signs of hypernatraemia.(
NO EDEMA)
·
Urinary buffers are necessary for effective
excretion of acid, because the minimum pH of the urine is only 4.0 to 4.5. Phosphate is the primary urinary buffer.
·
Aldosterone secretion is increased when plasma
concentrations of angiotensin II or potassium (K+) are increased.
·
Filtered Load = GFR / Px = 120 mL/min / 10 mg/mL
= 12 mg/min
·
Excretion = Ux * V = 10 mg/mL * 1.5 mL/min = 15
mg/min
·
Secretion = 15 mg/min − 12 mg/min = 3
mg/min
·
The intracellular Na+ concentration of renal
epithelial cells is pumped out of renal epithelial cells by Na-K pumps located
on the basolateral surface of the epithelial cells. The Na/H exchanger and the
Na-glucose transporter are located on the apical surface of the epithelial
cells. Na+ is transported from the peritubular spaces to the capillaries by
solvent drag.
·
The net glomerular capillary pressure (for
Starling forces) is equal to the glomerular capillary pressure minus the sum of
the plasma oncotic pressure and intrarenal pressure. Compression of the renal
capsule increases the intrarenal pressure and therefore decreases the net
capillary filtration pressure.
·
Net acid excretion = ([titratable acids] +
[NH4+] − 2 [HCO3−]) × urine volume per day
·
When water is filtered across the glomerulus,
the protein concentration (the oncotic pressure) within the capillaries
increases, which in turn increases the efficiency by which water reabsorbed
from the proximal tubule is returned to the circulatory system. If GFR
increases, it results in a larger increase in oncotic pressure. This in turn
increases the amount of water reabsorbed from the proximal tubule.
·
The distal nephron has a negative luminal
potential because it is poorly permeable to negatively charged ions. Therefore,
when Na+ is reabsorbed, negatively charged ions, primarily Cl−, lag
behind, producing a negative intraluminal
potential.
·
An increase in NaCl concentration occurs when
the amount of fluid flowing through the ascending limb increases because there
is less time available for the reabsorption of NaCl. The resulting increase in
Cl− concentration results in the release of adenosine from the macula densa. Adenosine constricts
the afferent arteriole resulting in a decrease in filtration and a return of
the flow rate within the nephron toward normal. This response is referred to as
tubuloglomerular feedback. If NaCl concentration decreases, for example, when
circulating blood volume decreases, the decreased Cl− concentration
results in the release of renin from granular cells of the juxtaglomerular
apparatus.
·
Nitric oxide dilates the afferent arteriole and
constricts the efferent arteriole, producing a rise in glomerular capillary
pressure (and glomerular filtration) without having much of an effect on renal
blood flow.
·
Prostaglandins, bradykinin, and dopamine all
increase renal blood flow. Cyclooxygenase inhibitors, such as aspirin, that
decrease prostaglandin synthesis may impair renal blood flow sufficiently to
exacerbate the effects of renal failure.
·
Phosphate is almost completely reabsorbed in the
proximal tubule, so its concentration decreases along the length of the tubule.
·
ANP increases Na+ excretion by decreasing the
amount of Na+ reabsorbed from the inner medullary collecting duct by decreasing
the permeability of the apical membrane of the collecting duct epithelial
cells. Less Na+ is able to enter the epithelial cells and therefore, less Na is
reabsorbed. ANP also increases Na+ excretion by increasing the filtered load of
Na+.
·
The proximal tubule reabsorbs approximately
two-thirds of the filtered water and two-thirds of the filtered Na+, Cl–, and
K+. Therefore, the concentration of these substances is the same at the
beginning and end of the proximal tubule. Because creatinine is not reabsorbed,
its concentration increases from the proximal to distal ends of the proximal
tubule. Phosphate, however, is almost completely reabsorbed in the proximal
tubule, so its concentration decreases along the length of the tubule.
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