Urinary System Flashcards
Functions of the kidneys
- regulation of water, inorganic ion balance, and acid-base balance
- removal of metabolic waste products from the blood and their excretion in the urine
- removal of foreign chemicals from the blood and their excretion in the urine
- gluconeogenesis
- production of hormones / enzymes
a. EPO (erythropoietin), which controls erythrocyte production
b. renin, an enzyme that controls the formation of angiotensin and influences blood pressure and sodium balance
c. PTH, which influences calcium balance
why is the right kidney lower than the left?
because of the liver
nephron
“functional unit”
~ 1 million / kidney –> can’t make more but can increase workload
renal cortex
outer layer
renal medulla
inner layer
series of tubules
capillaries
portal system
2 sets of arterioles + 2 sets of capillaries
types of nephrons
- juxtamedullary
2. cortical
juxtamedullary nephron
- 15%
- long nephron loop
- generate gradient in medulla needed for water reabsorption from collecting duct
- vasa recta
Cortical nephron
- 85%
- short nephron loop
- majority of filtration
- do not contribution to hypertonicity in medulla
- peritubular capillaries
juxtaglomerular (JG) apparatus
macula densa + juxtaglomerular (JG) cells
- important in regulation filtration rate
macula densa
- distal convoluted tubule (located)
- senses Na+ / Cl-
Juxtaglomerular (JG) cells
- afferent arteriole
- secrete renin
basic regnal processes
- glomerular filtration
- tubular reabsorption / secretion
- water conservation
glomerular filtration
creates a plasma like filtrate of blood
–> renal corpuscle
tubular reabsorption
removes useful solutes from the filtrate, returns them to the blood
- in the PCT and DCT
tubular secretion
removes additional wastes from the blood, adds them to the filtrate
- in the PCT and DCT
water conservation
removes water from the urine and returns it to the blood; concentrates wastes
- in the PCT, collecting duct, and loop of nephron
what substances are filtered + secreted but not reabsorbed?
drugs / toxins
what substances are filters and some of it is reabsorbed?
Na+ / water
what substances are filtered and completely reabsorbed?
glucose
renal corpuscle
glomerular capillaries + glomerular capsule
glomerular capillaries + podocytes = glomerulus
layers of glomerular filtration
- capillary endothelium
- basement membrane
- podocytes
LEAKY!!
glomerular filtration filters based on:
- size
2. charge
basement membrane
gel like negative charge: repels large, charged molecules
substances that are turned back during glomerular filtration
- blood cells
- plasma proteins
- large anions
- protein-bound minerals and hormones
- most molecules >8 nm in diameter
substances passed through the filter during glomerular filtration
- water
- electrolytes
- glucose
- amino acids
- fatty acids
- vitamins
- urea
- uric acids
- creatine
GFR
glomerular filtration rate
GFR average
125 mL/day
favoring filtration:
- PGC (glomerular capillary blood pressure)
opposing filtration:
- PBS (fluid pressure in Bowmen’s space)
- πGC (osmotic force due to proton in plasma)
average of PCG
60
net glomerular filtration pressure equation
PGC - PBS - πGC
PGC > PBS + πGC means
movement of fluid into capsule
vasomotion __
of the afferent and efferent arteriole alters PGC to change GFR
constrict afferent arterioles means
- decreased PGC
- decreased GFR
dilate efferent arterioles means
- decreased PGC
- decreased GFR
constrict efferent arterioles means
- increased PGC
- increased GFR
dilate afferent arterioles means
- increased PGC
- increased GFR
renal auto regulation (intrinsic control)
ability of nephrons to adjust blood flow in order to maintain GFR despite changes in blood pressure —> ordinary daily changes
intrinsic controls on regulation of GFR
- myogenic mechanism
2. tubuloglomerular feedback
myogenic mechanism
- smooth muscle contracts when stretched
- increased BP = increased stretch of afferent arteriole = increased vasoconstriction = decreased PGC = maintain GFR despite increased BP
tubuloglomerular feedback
- high GFR
- rapid flow of filtrate in renal tubules
- sensed by maculae densa via Na+ / Cl-
- paracine secretion –> adenosine
- constriction of afferent arteriole –> decreased PGC
- reduced GFR
effects of autoregulation
- when BP changes rapidly, GFR does not change much (maintains fluid/electrolyte balance)
- if no renal auto regulation:
MAP: 100 –> 125 mmHg
urine output would go from 1-2 L/day to 45 L/day
extrinsic control on regulation of GFR
- sympathetic nervous system
- when BP change is dramatic / persistent (strenuous exercise / shock)
- SNS = vasoconstrict afferent arteriole (also help redirect blood flow to heart, brain, muscles) = decreased PGC = decreased GFR
tubular reabsorption
- filtered loads are huge
- reabsorption of water, ions, nutrients, etc. is almost complete
- –> water and ions are regulated
- –> nutrients are NOT regulated
- reabsorption of wastes is incomplete –> excreted
- most reabsorption occurs in PCT (65%)
- 99% of filtrate is reabsorbed
- occurs by diffusion and thru transporters
- –> not regulated in the PCT
transport maximum
- substances needing protein carriers have a “transport maximum”
- if all transporters are occupied some solute won’t be reabsorbed and will appear in urine
- only occurs in a diseased state
tubular secretion
- to dispose of substances at higher rate than filtered load
- foreign chemicals (drugs) and toxins
- –> 80% of penicillin lost in 3-4 hours
- metabolic wastes (urea, uric acid, creatinine)
- H+ / K+
- via active transport (usually coupled to sodium)
- –> can also have transport maximum, foreign chemicals compete for same transporters
- most secretion is into proximal tubules (not regulated)
- -> except K+ and H+ are in the distal (regulated)
Na+ is regulated by ______ and ______ in the ______ during tubular _______
aldosterone and ANP in the DCT during tubular reabsorption
K+ is regulated by _____ in the ____ during tubular ____
aldosterone in the DCT during tubular secretion
water is regulated by _____ in the _____ during _____
ADH in the collecting duct during tubular reabsorption
water follows solute via _____
osmosis
Na+ determines amount of water in the extracellular fluid means
increased Na+ = increased water = increased blood volume = increased blood pressure
sodium reabsorption
- most Na+ is reabsorbed in the PCT (not regulated)
- Na+ reabsorption is regulated in DCT
- aldosterone builds Na+ channels and Na+/K+ pumps
- ANP inhibits Na+ channel activity
effects of angiotensin II
- widespread vasoconstriction (increase TPR)
- increased aldosterone = increase Na+ reabsorption in DCT
- increased ADH = increased water reabsorption in collecting duct
result of angiotensin II
when plasma volume drops, an increase in RAA reduces Na+ and water loss to increase BP
atrial natriuretic peptide (ANP)
increased BP/BV = stretch in right atria = increase ANP =
- afferent dilation & efferent constriction = increase GFR
- decreased aldosterone
- decreased ADH
- decreased Na+ reabsorption
- -> increase Na+ and water excretion
ANP result
when plasma volume increases, ANP increases Na+ and water loss to decrease BP
water reabsorption
- proximal tubule; water follows Na+ –> osmotic drage
- not regulated
- osmosis is ALWAYS the driving force for water
- regulation of water reabsorption in the distal nephron requires an osmotic gradient in the medulla
countercurrent multiplier
in loop of nephron = creates gradient in vasa recta
- effect is “multiplied” as move deep into medulla”
- urea from collecting duct contributes to increased osmolarity of ECF
countercurrent exchanger
maintains gradient
ascending limb (countercurrent multiplier)
- active transport of salt –> into medulla (ECF)
- impermeable to water
- water does not follow
descending limb (countercurrent multiplier)
- impermeable to salt
- permeable to water
- water moves out until concentration in/out are equal
higher protein diet leads to
increased urea = increase ability to concentrate urine
renal regulation of water
- osmotic gradient is used in collecting duct to concentrate urine
- –> gives water a reason to move
- presence of water channels in collecting duct is regulated by ADH
when is ADH secreted?
when blood osmolarity is high (dehydrated)
+ADH
increased number of Aquaporins in collecting duct = increased water reabsorption
- ADH
decreased number of Aquaporins in collecting duct = increased excretion (collecting duct is relatively impermeable to water)
what gland secreted ADH?
posterior pituitary
main function of ADH
regulate plasma osmolarity
renal regulation of potassium
- potassium is the main intracellular ion
- small changes in [K+] of ECF can cause lethal malfunction of excitable tissues
- K+ is absorbed in the PCT by diffusion
- excess K+ is secreted in the DCT (regulated by low)
norokalemia
- K+ concentrations in equilibrium
- equal diffusion into and out of cell
- normal resting membrane potential (RMP)
hypokalemia
- reduced extracellular K+ concentration
- greater diffusion of K+ out of cell
- reduced RMP (cells hyper polarized)
- cells less excitable
hyperkalemia
- elevated extracellular K+ concentration
- less diffusion of K+ out of cell
- elevated RMP (cells partially depolarized)
- cells more excitable
aldosterone
- regulates the secretion of K+ in the distal nephron by building pumps and channels
- cells are directly sensitive to K+ levels (no renin involved)
H+ gain
- generation of H+ from CO2
- production of acids from metabolism of proteins and other organic molecules
- gain H+ due to loss of bicarbonate in diarrhea or other non gastric GI fluids
- gain of H+ due to loss of bicarbonate in the urine
H+ loss
- utilization of H+ in the metabolism of various organic anions
- loss of H+ in vomit
- loss of H+ (primarily in the form of H2PO4- and NH4+) in urine
- hyperventilation
urine is usually ____
acidic
- except for strict vegetarians
buffers
- first line of defense
- short-term
- msec-sec
buffers buffering capacity
low
buffers response time
fast
respiratory
- via changes in CO2
- intermediate
- sec - min
respiratory buffering capacity
intermediate
respiratory response time
intermediate
renal
- via bicarbonate / H+ excretion
- long-term
- hours - days
renal buffering capacity
high
renal response time
slow
buffer systems ICF
- phosphates
- proteins
buffer systems ECF
- bicarbonate
- proteins
what happens when there is too much acid/base in the buffer system?
shift equilibrium = release or accept H+
respiratory system
CO2 + H2O –>
what happens when there is too much acid in the respiratory system?
hyperventilate to decrease CO2 = decrease H+
what happens when there is too much base in the respiratory system?
hyperventilate to increase CO2 = increase H+
renal regulation of pH
kidneys filter bicarbonate but CANT reabsorb it directly
renal regulation: when pH is balanced
filtered bicarbonate is recovered and “recycled” into new bicarbonate ion
what if blood is alkalotic?
bicarbonate ions that are filtered run out of H+ to recombine with = excreted
- more bicarbonate than H+
- not regulated = no active response = it just happens
Renal regulation: Excess H+
- after all filtered bicarbonate is gone, secreted H+ combines with phosphates and is excreted
- net gain of bicarbonate
- H+ excretion bound to HPO4-2
renal regulation: excess H+ w/ glutamine
- secrete H+ with ammonium
- net gain of bicarbonate
- H+ excretion bound to NH3-
- urine pH can be as low as 4.5 then transporters stop working
acidosis
- pH < 7.35
- decrease CNS function (confusion, disorientation, coma)
- pH < 7.0 quickly fatal
alkalosis
- pH >7.45
- increase muscle contraction (spasms, convulsions, paralysis)
- pH > 8.0 quickly fatal
respiratory
change in pH caused by change in CO2
metabolic
change in pH not caused by change in CO2
respiratory acidosis problem
increased CO2
respiratory acidosis causes
- hypoventilation
- emphysema
respiratory acidosis respiratory compensation
increase ventilation
respiratory acidosis renal compensation
increase H+ excretion
- bound to H2PO4- or NH4+
respiratory alkalosis problem
decreased CO2
respiratory alkalosis cause
hyperventilation
respiratory alkalosis respiratory compensation
decrease ventilation
respiratory alkalosis renal compensation
increase bicarbonate excretion
- nothing to bind to
metabolic acidosis problem
increased H+ or decreased bicarbonate
metabolic acidosis causes
- diarrhea
- diabetes
- exercise
metabolic acidosis respiratory compensation
increase ventilation
metabolic acidosis renal compensation
increase H+ excretion
- bound to H2PO4- or NH4+
metabolic alkalosis problem
decreased H+ or increased bicarbonate
metabolic alkalosis causes
- vomiting
- increased aldosterone
- exchange K+ for Na+ first then will use H+
metabolic alkalosis respiratory compensation
decrease ventilation
metabolic alkalosis renal compensation
increase bicarbonate excretion
- nothing to bind to
renal clearance
- the volume of plasma from which all of a substance is removed (cleared by the kidney per minute
- also a measure of efficiency of kidneys
equation of renal clearance
C = [U] x V / [P]
clearance is used to determine
- GFR
- renal plasma flow
- handling of new substances
inulin
polymer of fructose from plants
- must infuse at a constant rate
- is used to measure GFR with renal clearance
what is used for a more practical way for renal clearance?
Creatinine
Creatinine
- produced by muscles at a constant rate
- freely filtered
- not reabsorbed
- only slightly secreted
- measuring creating clearance gives a 10% overestimate of GFR
PAH
para-amino hippuric acid
clearance of PAH
- infused like inulin
- PAH is completely secreted and all removed in one pass
- so clearance of PAH is about renal plasma flow
- decrease C PAH = decrease renal plasma flow = blockage of renal artery
urine
- shade of yellow
- clear
specific gravity range
- 002 - 1.030
- used to estimate osmolarity
osmolarity range
about 80 - 1200 mOsm/L
pH range
4.5 - 8.2
urine volume range
1-2 L/day
what shouldn’t be in urine
- protein
- blood
- ketones
- glucose
- bilirubin
- urobilinogen
- nitrites
- leukocytes
protein
- trace amounts okay
- kidney disease
blood
- kidney stones
- infection
ketones
- product of fat metabolism
- fasting, keto diet, increased diabetes
glucose
hyperglycemia, increased diabetes
bilirubin
- increase in liver disease
- metabolite of Hb degradation, normally lier puts in bile
urobilinogen
from eating fatty foods/meals
nitrites
- increased infection
- metabolite of bacteria
leukocytes
- increased infection
- WBC’s
UTI
- increased WBC’s
- bacteria
- +/- nitrites
glomerular nephritis
- increased WBC’s
- increased protein
- pus
bilirubin formation and excretion
- normally removed by liver and put in bile
- small amounts are normal in urine
- increased by GI tract during fatty meals
diuresis
> 2L urine / day
diuretic
any chemical that increases urine volume
diuretic: caffeine
dilates afferent arteriole = increased GFR
diuretic: alcohol
inhibits ADH = increased water excretion
diuretic: nicotine
antidiuretic = increase ADH release
diabetes mellitus (osmotic diuresis)
- failure to reabsorb glucose –> Tm
- more water is excreted with glucose
- water follows glucose into urine
diabetes insipidus (water Diuresis)
- failure of posterior pituitary to release ADH or failure of kidney to respond to ADH
- water permeability in collecting duct is low
- increased water loss
- 25 L / day
what type of muscle is the detrusor
smooth muscle
detrusor innervation type
PSNS causes contraction
detrusor during filling
inhibited
detrusor during micturition
stimulated
what type of muscle is the internal urethral sphincter
smooth muscle
internal urethral sphincter innervation type
SNS causes contration
internal urethral sphincter during filling
stimulated
internal urethral sphincter during micturition
inhibited
what type of muscle is the external urethral sphincter
skeletal muscle
external urethral sphincter innervation type
somatic motor causes contraction
external urethral sphincter during filling
stimulated
external urethral sphincter during micturition
inhibited
