Review Sheet 2 for Test #3
Biology 2213
Dr. James Adams
THE URINARY SYSTEM
--
Chap. 25
Two Major Functions:
1. Osmoregulation
2. Excretion of Nitrogenous Wastes (internally produced)
Auxiliary Functions:
1. Release of renin from juxtaglomerular cells of afferent arteriole (regulation of BP)
2. Release of erythropoietin
3. Gluconeogenesis
Urinary System Anatomy -- refer to your laboratory practical AStructures to Know@ sheet,
and remember, as always, you are responsible for knowing the epithelial linings/muscle
in the walls of the various organs
Gross Anatomy
1. Kidney location, Renal capsule, Adipose capsule, Renal fascia
2. Cortex and Medulla (with renal pyramids/columns), Pelvis (with calyces), renal hilus
3. Renal Artery and Vein, Interlobar arteries and veins, Arcuate arteries and veins
4. Ureters, Bladder (with trigone; special
tri-layered detrusor muscle), urethra, internal and
external urethral sphincters
Microscopic Anatomy -- of the Nephron (Renal Tubule System); >1,000,000 per kidney
1. Renal Corpuscle = Glomerulus + Bowman=s Capsule (with
podocytes/filtration memb)
2. Proximal/Distal Convoluted Tubules
(PCT/DCT)
3. Loop of Henle (Descending/Ascending limbs/arms; thin/thick segments)
4. Collecting/Papillary Ducts (form renal pyramids)
5. Blood flow (a portal system)
-- Afferent/efferent arterioles (for glomerulus); peritubular
capillaries; form vasa recta around Loop of Henle in JM
nephrons*
6. Juxtaglomerular (JG) Apparatus -- involves the JG cells in afferent arteriole and macula
densa cells in DCT
Types of nephrons: Cortical (85%); *Juxtamedullary (15%) with long Loop of Henle
--
only
juxtamedullary important for concentrating urine
Physiology
Vascular Resistance in microcirculation around nephron: two arterioles (afferent & efferent)
greatly control blood pressure in the subsequent capillary beds (glomerulus [very
fenestrated]
and peritubular capillaries); efferent narrower than afferent which reinforces
higher BP
in glomerulus than most capillary beds in the systemic circulation
--
necessary for filtration.
Urine Formation -- three processes involved: filtration, tubular reabsorption and secretion.
I. Glomerular Filtration is passive; through filtration membrane
Blood pressure forces about one fifth of plasma through (125ml/min; 180 L/day)
Small molecules (H20, glucose, amino acids) pass freely; molecules larger than 5 nm do
not enter filtrate; large proteins keep water in bloodstream.
Blood Pressure higher in glomerulus than other caps.; generates lots of filtrate
Need to know concept of Net Filtration Pressure (NFP) and Glomerular Filtration Rate
(GFR)
and their effects on filtrate formation
Controls of GFR:
1. Intrinsic (autoregulation)
-- maintains GFR in face of widely fluctuating systemic BP
a. Myogenic mechanism
b. Tubuloglomerular feedback mechanism
-- involves Juxtaglomerular Apparatus
Macula densa cells respond to filtrate flow rate/osmotic concentration
When flow rate slow/osmotic concentration low, promote vasodilation of
afferent arterioles; also sets renin-angiontensin mechanism (see below)
into motion
When flow rate high/concentration high, promote JG cells of afferent
arterioles to generate vasoconstriction
2. Extrinsic controls -- neural and
hormonal
a. Sympathetic Nervous System Controls
-- overall effects discussed previously,
Extreme stress results in great decline of GFR due to significant constriction
of
afferent arterioles; directly stimulates JG cells to release renin (see
directly below)
b. Renin-Angiotensin Mechanism
(obviously tied in with other influences)
Influences systemic BP (and therefore indirectly GFR as well)
Remember, angiotensin potent vasoconstrictor
-- main thrust is to raise
systemic BP by constriction of systemic arterioles
Angiotensin has
various effects on GFR, besides rise in systemic BP:
i. Stimulates release of aldosterone from adrenal cortex, ADH from hypothalamus
(increases
reabsorption of both NaCl and water; which reduces flow in DCT)
ii. Stimulates efferent arteriole to constrict more than afferent -- maintains GFR
and reduces filtrate flow which allows for more fluid reasorption back into
peritubular capillaries
iii. Also targets glomerulus "directly" and reduces GFR
Know
different stimuli which set R-A mech. in motion (see top of pg. 974).
Take home message: nearly
constant GFR can be maintained even in BP varies
between 80 and 180
II. Tubular Reabsorption
180 liters of filtrate produced daily, 1.5 liters of urine released. Approx. 99% of all
filtrate must be reabsorbed from filtrate into peritubular capillary blood. No surprise
that kidneys (<1% of body weight) use about 20-25% of O2 (and therefore ATP)
at rest. Virtually all organics reabsorbed; ions
(therefore water) under specific controls.
You will need to know the following concepts (most of which you=ve already been
exposed to at
an earlier date): Active transport (mostly of Na+), co-(sym-)transport,
passive reabsorption, solvent drag
Transport maximum B each substance that is actively or cotransported can only be
transported at a rate which is based on the flow rate and number of transport proteins
Reabsorption in different parts of the Nephron:
1. PCT (with microvilli)
-- majority of reabsorption from here. All organics, approx
65% of Na+ (and therefore water), and selected portions of other ions.
Also almost all uric acid and some urea (!)
2. Loops of Henle
-- descending limb permeable to water; ascending limb is not
(important for concentrating urine, described below); solute transport not
coupled to osmosis (water does not follow the solutes directly in this case)
By end of Loop of
Henle, 25% more of Na+, 10% of water, 35% of Cl- reabsorbed
3. DCT and Collecting Duct
-- 25 % of volume, and 10% of salt remain
Nearly all of both the water and salt can be reabsorbed as needed
Permeability to water completely dependent on ADH presence; lack
of ADH
means lack of water reabsorption from these regions
Reabsorption of Na+ (and secretion of K+) dependent on aldosterone release
Remember also that ANF (or ANP) released from the atria when venous return is
high inhibits aldosterone release, and also increases GFR
Nice summary diagrams: pgs.
974 - 977
III. Tubular Secretion
This is the ability to put materials (in some cases replace materials) from peritubular
capillary blood into the filtrate in the nephron. This includes uric acid and some urea
that was reabsorbed,
manipulation of K+ and/or H+, and Cl- and/or
HCO3-
(involved in acid base balance)
Controlling Urine Concentration
When copious amounts of water drunk, need to release dilute urine
However, we are terrestrial, and much more frequently we face the need to conserve
water (concentrate urine) than get rid of
excess water.
Two nephron parts vital to concentrating urine: Loops of Henle and Collecting Ducts
Remember salts pumped from ascending limb (which draws some water from
descending limb);
this makes the tissue of the medulla very salty (high osmotic
concentration); in other words, as
you descend into the medulla, there is an
increasing salt gradient. As fluid passes through the collecting ducts,
thereby
descending through the medulla, increasing amounts of water can be drawn
out (assuming ADH is present). Additionally, the collecting ducts are permeable
to urea and some urea diffuses out, adding to the medullary solute concentration
gradient. In other words, we retain some urea, which sounds weird, but it helps
with the
ability to concentrate the urine.
Renal Clearance: A measure of the amount of substance released compared to the
amount of the same substance filtered; gives an idea of the reabsorption/secretion
capabilities of the nephrons
Urine Characteristics:
Color/transparency; odor; pH (varies anywhere from 4 to 8)
Chemical Composition -- most abundant components: water, urea, sodium in that order
many other ions
Any organics in the urine (red blood cells, proteins, etc.) indicate some pathology
Rest of Urinary System covered above -- Ureters, Bladder, Urethra
Know about expansion capabilities of Bladder, and Micturition (Urination;
involving
involuntary internal urethral sphincter [at bladder] and
voluntary external urethral
sphincter [at abdominal wall])
FLUID, ELECTROLYTE, and ACID-BASE BALANCE -- Chap.
26; on Test 4
Almost entire chapter is review of
information from previous chapters; very little new
information, just put together in a different fashion than previously.
Body Fluids -- Water
Total body water represents typically $50% of body mass; most in infants, least in ederly
Adult males avg. 60%; females 50% (fat is the least hydrated tissue)
Fluid Compartments: (numbers for a 70 kg man)
1. Extracellular Fluid Compartment (ECF) -- 15 liters:
subdivided into plasma (3 liters) and interstitial fluid (several types: 12 liters)
2. Intracellular Fluid Compartment (ICF) -- 25 liters
Main differences between compartments are the solutes; grouped into electrolytes
(ions) and non-electrolytes (includes many organics, such as protein)
Understand concept of milliequivalents for electrolytes (ionic compounds)
You should also know main solutes in all compartments, and therefore the differences
between them; for example, the main extracellular cation is . . .? . . . the main intracellular
anion is . . .? (Figure 26.2, pg. 992)
Fluid Movements Between Compartments
The main concept to remember here is that all compartments will more or less remain
isotonic to one another; any momentary fluctuation in the solute content in one
compartment is offset by osmotic movements of water
-- thus, volume of ICF is
determined by solute concentration of ECF
Exchanges:
Between plasma & interstitial fluid -- across capillary walls (remember
capillary
dynamics)
Between interstitial fluid and ICF -- selectively across cell membranes
Only plasma circulates, so it is the ultimate link in exchanges between compartments
I. Water Balance -- Input must equal output
Inputs -- drink, food, cellular respiration (and other metabolic processes)
Outputs -- urine, sweat, feces, insensible losses (respiratory surfaces, skin)
Regulation of Intake -- the thirst mechanism
Involves the hypothalamus -- remember, the BBB is leaky here, so that the
hypothalamal receptors can sample the plasma contents; thirst triggered when
osmotic content of plasma elevated, which causes hypothalamal osmoreceptors
to lose water, which depolarizes them
Salivary glands reduce water output
-- dry mouth
Thirst quenched almost immediately -- moistening of upper GI tract mucosae and
stretch receptors in stomach involved. Prevents overhydration
Regulation of Output
We have obligatory water losses (insensible, fecal
and a certain minimal urine loss)
Renal concentrating mechanisms are the main way to conserve water
As you will
see, water balance very much tied to Na+ balance as well (where
solutes go, water follows).
Disorders B know about dehydration and hypotonic hydration
II. Electrolyte Balance -- will examine Na+, K+, and Ca+2 mainly (though this will
involve Cl- and HPO4-2)
A. Central Role of Na+
-- Most abundant extracellular cation, and only one exerting
significant osmotic pressure, which means it is central in moving water around
between compartments
(Don=t forget, Na+ also plays a major role in electrical gradients)
Regulation of Na+ Balance
-- interestingly, virtually no chemoreceptors that respond
specifically to Na+ have been found yet in the body
1. Aldosterone is, of course, a key player; stimulators of aldosterone release include
i. Angiotensin
ii. Elevated K+ levels
(Addison=s disease/pica)
2. ANP
3. Other Hormones
-- Female Sex Hormones
4. Baroreceptors in the Circulatory System
-- in essence, these are Na+ receptors,
since blood volume is dependent on solute volume
Remember, besides pulling water around, Na+ typically also pulls Cl- around
B. Potassium Balance -- very much tied to acid base balance, as shifts in
H+ often offset by opposite direction shifts in K+. With acidosis, ECF K+ goes up;
with alkalosis, K+ re-enters cells (H+ exits)
You should know
the reasons why this happens! (See acid-base balance below)
Regulation of K+ Balance
-- main site: cortical collecting ducts
Main thrust of renal mechanisms is to excrete K; faced with shortages the kidneys
have a very limited ability to conserve K+, and K+ may be lost even when needed.
Factors involved: K+ levels directly; aldosterone
C. Calcium (and Phosphate) Balance -- 99% of body=s calcium is in bones (as calcium
phosphate salts), yet ionic calcium necessary for many physiological events
Regulation of Ca+2 Balance
-- two hormones, PTH and calcitonin, of which PTH is far
more crucial (you already know what these hormones do!)
Calcitonin
(from thyroid) targets mainly bones (osteoblasts)
PTH targets: bones (osteoclasts), small intestine (vitamin D) and kidneys (reabsorp.
from nephrons)
Osteoclasts/-blasts working on bones will also release/deposit phosphate ions
from/to
bones, so PTH and calcitonin are majorly involved in phosphate balance as well
D. Regulation of Anions -- know about Cl- and HPO4-2 (phosphate); be aware that,
like potassium, chloride ions are also involved in acid-base balance by being shifted
with bicarbonate (HCO3-)
III. Acid-Base Balance -- pH balance so crucial to normal metabolic functioning
ICF typically at pH 7; plasma varies but typically slightly alkaline
Most H+ generated as metabolic by-products
Regulation of H+ Balance: three main mechanisms
1. Chemical Buffer Systems -- involves
weak acids and associated weak bases
a. Bicarbonate Buffer System
-- the only important ECF buffer system (though there
is some protein buffering in plasma
b. Phosphate Buffer System
-- only important in ICF, though protein buffering also
important in ICF
c. Protein Buffer Systems
-- amine (base) and carboxyl (acid) ends; also important
in ICF
2. Respiratory Mechanisms --
two times buffering capabilities of all chemical buffers
Clearly, this is directly tied to the bicarbonate buffering system
Changes in AVR in a healthy individual can go well beyond compensating for most
pH fluctuations
3. Renal Mechanisms -- only kidneys can actually remove metabolically produced acids
Mainly this involves regulating bicarbonate ion levels (conserving and generating new
ones; understand concept presented in Fig. 26.12, pg. 1007)