_Urinary

Anatomical illustrations by from "Art Explosion 40,000," copyright Nova Development Corporation,
Calabasas, CA.; used under terms of license granted to Dr. J.V. Aliff.
 

Chapter 25 - Urinary Study Guide, p. 960, 8th ed.
 

PATH OF URINE

The collecting ducts empty into the renal pelvis -----> minor calyx (funnel-like)
-----> major calyx -----> pelvis -----> ureter -----> peristalsis -----> urinary bladder
- ----> urethra -----> out. The bladder has an involuntary parasympathetic
innervated internal sphincter, and a voluntary somatic innervated external sphincter.
See p. 998,1025, 7th ed.; 961-964, 8th ed.

The Nephron - General Functions (See p.1004, 7th ed.; p. 965, 8th ed.)

1. Glomerulus - all are found in the cortex of the kidney, they are capillary balls
   (instead of a bed) surrounded by a hollow Bowman's Capsule of squamous cells. The
   capillary (squamous endothelial) cells are fenestrated (with window-like holes in the endothelial cells). 180-200
   liters a day of initial filtrate forced by the blood pressure (pressure filtration - the
   same process basically as interstitial fluid/lymph formation) through the fenestrated
   capillaries, slit membrane and filtration slits of Bowman's Capsule into its cavity. If
   the glomerular filtration rate (GFR) drops because of a drop in B.P., oligouria
   (less than 250 ml/day) or anuria (less than 50ml output per day) results. The initial
   filtrate has a great deal of useful water and nutrients in it that must be reclaimed by
   the remainder of the tubule. All glomeruli are found in the outer cortex of the kidney.
   An afferent arteriole carries blood to the glomerulus and a smaller efferent arteriole
   carries blood away to the peritubular capillary bed, incurring a fairly high B.P. in the
   glomerulus. How do generalized vasoconstriction of blood vessels, or vasoconstriction
   of the efferent arteriole effect GFR? How do aldosterone, ADH and atrial natriuretic
   hormone effect GFR? Review hormones.

   2. Proximal Convoluted Tubule - reabsorption begins in this tubule composed of
   tall cuboidal cells with a "brush border" of pinocytic vesicles. The ATP powered
   process of active transport moves glucose, amino acids, and salts into the tubule
   wall and then into the peritubular capillary bed (blood). Water passively follows
   the solutes being transported back into the blood, Glucose exceeding a blood
   concentration of 200 mg/% spills over into the urine because active transport pumps
   are saturated at that level. The secretion of H⁺ and NH₄⁺ also occur here. See
   p. 1011-1012, 7th ed.; p. 977, p. 980-883, 8th ed.

   3. Loop of Henle - See p. 1017-1019, 7th ed. p. 977, p. 980-883, 8th ed.

   a. Descending limb - this tubule region descends into the deeper and salty medulla
   of the kidney. Water is pulled out osmotically by high salt and urea concentrations in
   the medullary tissues.
   b. Ascending (thick) limb - this tubule ascends toward the cortex. Salts including Na⁺, K⁺,
   and Cl⁺ are extruded from the ascending limb to produce the high salt concentration of
   the medullary tissues. Excess salts (above the high medullary level) are actively
   transported back into the descending limb. The wall of the ascending limb is
   impermeable to water moving out possibly because of a lack of aquaporin water channel
   molecules in their membranes.

4. Distal Convoluted Tubule - important processes occur here:
    a. Tubular Secretion - some wastes or extraneous materials like urea, creatine
    from muscle contraction, and penicillin are removed from the capillary bed directly
    into the DCT and PCT.

    b. Ion Exchange and Secretion - the pH of the blood can be adjusted by
    exchanging ions with the filtrate in the PCT and DCT; i.e., an H⁺ (hydrogen) ion
    for a Na⁺ (sodium) ion and HCO₃^- (bicarbonate) ion, or an NH₄⁺(ammonium)
    for an HCO₃^-ion.

The NH₄⁺ ion is made from NH₃ derived from the deamination of amino acids
(see digestion) and a H⁺ ion from the blood. The ammonium ion then reacts with bicarbonate ion in the filtrate to make (NH₄)₂CO₃ (ammonium carbonate) that contributes to the smell of fresh urine. Is this a neutralization reaction?

As urine decomposes, the ammonia is released as a gas. Hydrogen ions also react with
(HPO₄^-2) monohydrogen phosphates in the filtrate to make the urine less acidic.
Nevertheless, urine can be 1000 times greater in acid than the blood.

That would make the urine have a low pH of ______?

Where the DCT winds back by the glomerulus/Bowman's Capsule, a
juxtaglomerular apparatus of cells of the outer wall of the afferent arteriole and
cells of the DCT called the macula densa occur. The JG apparatus in the wall of
the afferent arteriole apparatus secretes an enzyme called renin if the blood pressure
is low. The renin causes the 2-step formation of angiotensin I in the kidney blood
and then angiotensin II in the lungs, the latter made from AT I by angiotensin
converting enzyme, ACE. The resulting generalized vasoconstriction and that occurs
more in the efferent arteriole than the afferent arteriole raises blood pressure and
causes the adrenal gland to release aldosterone that causes the collecting duct to
reclaim more salt, the water naturally following passively to increase blood volume
and pressure. If the macula densa detects decreased flow and decreased NaCl
in the DCT, it causes the afferent arteriole to dilate, resulting in an increase of GFR.
See p. 1005, 7th ed.; p. 977, p. 980-883, 8th ed.

The sympathetic nervous system constricts the afferent arteriole to decrease
glomerular filtration rate in flight-fight.

Why do people with excessive adrenal cortical hormone secretions have high blood
pressure and why are they called salt retainers?

Review question: Using this material and that from the endocrine and heart chapters,
list and define 5 chemotherapy approaches to lowering blood pressure.

Why do low aldosterone (like Addison's Disease) secreting patients have low blood pressure
and why are they called salt wasters?

5. Collecting duct - the collecting duct forms in the cortex and descends into the
salty medulla. Again water is pulled out osmotically. A posterior pituitary hormone
called the antidiuretic hormone (ADH) causes the collecting duct to be permeable
to water moving back towards the blood by placing more aquaporin water channel
molecules in their membranes.. Aldosterone stimulated reabsorption of Na⁺
occurs here. Alcohol causes a decrease in ADH secretion. See p. 1024-1027, 7th ed.; p. 980-883, 8th ed.

Label as appropriate.

Why would you "pee like crazy'" if you had a deficiency of ADH?
 

Hemodialysis - this treatment allows most small particles (molecules or ions) to
cross the membrane in either direction, but large particles are held on one side. The
kidney dialysis machine is used to keep patients alive while they are waiting for a
transplant.

There is no Urea and potassium in the bath solution but the solute particle numbers
(concentrations) are balanced for other salts and glucose. Why does the albumin stay
in the blood? Can you remove all the urea this way?

Walking (continuous peritoneal) dialysis  uses abdominal cavity membranes to produce
waste. A bath solution is introduced into the abdominal cavity twice or more times daily
and removed likewise.

A renal calculus is a stone composed of calcium phosphate (as in excess PTH
secretion or Ca⁺⁺ from diet), calcium oxalate or uric acid (as in gout). Excess blood
acidity or alkalinity, and liver disease can cause stones.Math instructors
are good at working these out.

SOME NORMAL URINE CONTENTS/ 24 hours - See the Mareib lab manual and p. 1021, 7th ed.; p. 985, 8th ed.

1. Urea - 25 - 35 g
2. Creatine - 1.6 g
3. Uric Acid - 0.4 - 1.0 g
4. NaCl - 15 g
5. KCl - 3.3 g

1. Increased NaCl in urine - Addison's Disease or hyposecretion of aldosterone.
2. Increased KCl in urine - hypersecretion of aldosterone, adrenal cortical
   hyperplasia, and some cases of Cushings Disease.
3. Increased albumin or proteins - toxic shock, tumors, or high blood pressure
   damages the glomerular filtration membrane.
4. Glucose - diabetes mellitus or high sugar diet.
5. RBCs or Hemoglobin - sickle disease, infections, kidney stones, or
   glomerulonephritis.
6. WBCs - infections
7. High ketones - weight loss, diabetes mellitus. Fat breaks down to produce
   ketones.
8. Low pH - blood acidosis due to lactic acid, from anaerobic metabolism, acetoacetic
   acid from fat breakdown, high protein diet (causes high stomach acid and breakdown
   of amino acids yields keto acids), or respiratory acidosis.
9. High pH - conversely a low protein or vegetarian diet could produce very low
   acidity in the urine (pH >7). Note: low acid and high glucose levels can encourage the
   growth of bacteria in the bladder and cause cystitis.
10. Bilirubin, urobilinogen - due to jaundice.
11. Increased NH₄⁺ - due to liver failure, high protein diet, high stomach acidity, or blood acidosis.

Acute - sudden onset
              Oligouria - less than 250 ml urine made/day (adult).
              Anuria - less than 50 ml/day.

Chronic - slower, gradual onset
        1.    Diminished Renal Reserve - up to 75% of nephrons are
                nonfunctional.
        2.    Renal Insufficiency - between 75% and 80% of nephrons are
                nonfunctional. Oligouria is seen.
        3.    End Stage Renal Failure - 90% or more of nephrons are lost. Blood
                urea nitrogen level (BUN) is very high. Anuria is seen when less
                than 50 ml are produced/day (adult).

EMBRYOLOGICAL DEVELOPMENT - See p. 1029, 7th ed.; p. 988, 8th ed.

A prescribed series of kidney types develops in the human embryo.

1.  A pronephric kidney with funnel tubules opening from the
thoraco-abdominal cavity (undivided by a diaphragm at this stage)
of the embryo.  There is no direct connection to the blood circulatory
system and the system seems designed simply to bail out excess water;
waste removal would be secondary consideration.  This kidney is
always the first to develop in an embryo, but it does not function,
appearing cephalically in the thoracoabdominal cavity.  The pronephric
kidney and duct disappear as the next mesonephric kidney appears.

2.  The mesonephric kidney appears further caudally in the
thoracoabdominal cavity.  At this stage the kidney tubule structure is like
modern fishes and amphibians.  In the mammalian embryo, one sees a
non-functional oviduct (lateral) with a gonad (median) which develops
in conjunction to the mesonephros.  This is significant because the
mesonephros and its duct disappear (normally) in the female, the oviduct r
emains; in the male the mesonephric duct becomes the vas deferens and
the oviduct disappears along with the mesonephros.  The embryonic
mesonephros has glomerular capillaries in Bowman's capsules
(see significance below) and cavity funnels as well.  In general this kidney
is better designed for waste removal and water/nutrient reclamation than
the pronephros.  Notice that it is associated with a cloaca - a common
excretory and reproductory chamber.

3.  The typical bean shaped metanephric kidney forms last and further
down in the abdominal cavity from a separate block of mesoderm not
connected to the mesonephros except by a ureter duct at the distal end
of the mesonephric duct where the prostate and seminal vesicles later a
appear.  The tubules all have glomerular capillary bulbs and a capillary net
which surrounds the nephron tubule.  In general this kidney is even better
designed for waste removal and water/nutrient reclamation than the
mesonephros.  It is the final stage kidney of reptiles, birds and mammals.

There is also a precise sequence of development of nitrogenous wastes.
Nitrogenous wastes are produced by deamination (removal of nitrogen)
from amino acids (building blocks of proteins), with ammonia (NH₃)
the first (pronephros stage), the less toxic urea (NH₂-CO-NH₂) second
(mesonephros), the third is characterized by a rise in uric acid production
(early metanephros stage, reptilian), and the fourth, by a return of urea
as the primary waste excreted (mammalian metanephros).
 

Study Questions

1. Why do kidney dialysis patients have high potassium levels before treatment?
2. What are the dangers of high potassium level? See the digestion and heart
   chapters.
3. Compare and contrast the conditions and symptoms of diabetes mellitus (acute)
   and diabetes insipidus (see digestion chapter).
4. Why do people with excessive adrenal cortical hormone secretions have high
   blood pressure and why are they called salt retainers?
5. Why do low aldosterone-secretors have low blood pressure and why are they called salt
   wasters?
6. Describe the sugar diabetes disease processes which produce the symptoms
   of glucose and ketones in the urine. Why is each present?
7. What may cause urine to contain a high level of protein?
8. What happens in each section of the nephron? Focus on what is transported
   and how it is transported into or out of the nephric filtrate?
9. What is "shock kidney?"

Email:john.aliff@gpc.edu