renal system Flashcards
functions of kidneys
regulating total water volume and solute conc. in water
regulating ECF ion conc.
acid-base balance
removal of metabolic wastes, toxins, drugs
activation of vit. D
gluconeogenesis
renin and EPO secretion
minor calyces
drain pyramids at papillae
major calyces
collect urine from minor calyces
empty urine into renal pelvis
urine flow
renal pyramid->minor calyx->major calyx->renal pelvis->ureter
nephron
structural and functional units that form urine
contains renal corpuscle and tubule
mostly found in renal cortex
renal corpuscle
contains glomerulus and Bowman’s capsule
Bowman’s capsule
parietal layer=simple squamous epithelium
visceral layer= podocytes
podocytes
foot processes that cling to BM and allow filtrate to pass into capsular space
PCT
cuboidal cells w/ dense microvilli and large mitochondria
secretion and absorption
site of most reabsorption (glucose, AA, Na+, water, ions, uric acid, urea)
secrete H+ into filtrate
distal descending limb of loop of henle
aka thin limb
simple squamous epithelium
water can leave, solutes cannot
higher osmolarity
ascending limb of loop of henle
thick and thin limb
cuboidal to columnar cells
water cannot leave, solutes can
more dilute
DCT
cuboidal cells
secretion
in cortex
principal cells
in collecting ducts
sparse
short microvilli
maintain water and Na+ balance
intercalated cells
in collecting ducts
cuboidal cells
abundant microvilli
A and B cells that both help maintain acid-base balance
collecting ducts
receive filtration from many nephrons
run through pyramids
fuse together to deliver urine through papillae into minor calyces
reabsorption hormonally regulated (ADH, aldosterone, ANP, PTH)
cortical nephrons
85% of nephrons
mostly in cortex
juxtamedullary nephrons
long nephron loops deeply invade medulla
important in production of concentrated urine
glomerulus
specialized for filtration
blood goes into afferent arteriole->glomerulus->efferent arteriole
high BP due to large diameter of afferent arterioles
Bowman’s capsule receives filtrate from glomerulus
peritubular capillaries
low BP
porous
absorption of water and solutes
empty into venules
cling to adjacent renal tubules in cortex
vasa recta
long, thin-walled vessels parallel to long nephron loops of juxtamedullary nephrons
arise from efferent arterioles serving juxtamedullary nephrons
formation of concentrated urine
macula densa
tall, closely packed cells of ascending limb
chemoreceptors sense NaCl content of filtrate
granular cells
aka juxtaglomerular cells
enlarged, SM cells
contain enzyme renin
mechanoreceptors sense BP in afferent arteriole
extraglomerular mesangial cells
in juxtaglomerular complex
b/w arteriole and tubal cells
interconnected w/ gap junctions
pass signals b/w macula densa and granular cells
glomerular filtration
no metabolic energy required
hydrostatic pressure forces fluids and solutes through filtration membrane
filtration membrane
porous membrane b/w blood and interior or glomerular capsule (water and solutes smaller than plasma proteins)
made up of fenestrated endothelium, BM, and podocytes
hydrostatic pressure in glomerular capillaries
glomerular BP
chief force pushing water and solutes out of blood
55 mmHg due to efferent arteriole being high resistance
promote filtrate formation (outward force)
hydrostatic pressure in capsular space
inhibit filtrate formation (inward force)
pressure of filtrate in capsules
15 mmHg
colloid osmotic pressure in capillaries
inhibit filtrate formation (inward force)
pull of proteins in blood
30 mmHg
net filtration pressure
sum of forces
55 mmHg forcing out
45 mmHg opposing=net outward force of 10 mmHg
GFR
volume of filtrate formed per min by both kidneys (120-125 mL/min)
directly proportional to NFP, total surface area available for filtration (controlled by glomerular mesangial cells), filtration membrane permeability
decreased GFR triggers renin release in order to increase GFR
intrinsic controls
maintain GFR of kidneys when MAP in range of 80-180 mmHg
act locally within kidney
myogenic and tubuloglomerular (involves macula densa cells) mechanism
extrinsic controls
maintain systemic BP
nervous and endocrine mechanisms that maintain BP
take over if BP <80 or >180 mmHg
decreased BP->release of NE by SNS and E by adrenal medulla->vasoconstriction->increase BP
OR decreased BP->constriction of afferent arterioles-> decreased GFR->increase BV and BP
myogenic mechanism
intrinsic control
increased BP->constriction of afferent arterioles-> restricts BF into glomerulus (protects glomerulus from damaging high BP)
decreased BP->dilation of afferent arterioles
RAAS
extrinsic control
stimulate renin release via granular cells by SNS, macula densa cells when NaCl filtrate concentration is low, or reduced stretch of granular cells
other extrinsic controls
adenosine
prostaglandin E2
intrinsic angiotensin II
form concentrated urine
juxtamedullary nephrons and vasa recta
juxtaglomerular apparatus
macula densa cells
juxtaglomerular cells
extraglomerular mesangial cells
osmosis
reabsorption of water aided by aquaporins present in PCT (obligatory water reabsorption)
aquaporins present in collecting ducts only if ADH present (facultative water reabsorption)
solute concentration
increases in filtrate as more water is reabsorbed
transport maximum
reflects number of carriers in renal tubules available for every reabsorbed substance
when carriers saturated, excess excreted in urine (glucose)
ADH
causes principal cells of collecting ducts to insert aquaporins in apical membranes (aids in water reabsorption)
aldosterone
targets principal cells and DCT
promotes synthesis of apical Na+ and K+ channels and basolateral Na+-K+ ATPase for water reabsorption (water follows)
increases BP and decreases K+
ANP
decreases Na+ (decreases BV and BP)
PTH
acts on DCT to increase Ca2+ reabsorption
tubular secretion
in PCT
K+, H+, NH4+, creatine, organic acids, HCO3-
disposes of drugs
eliminates and passively reabsorbs urea and uric acid
rid body of excess K+
controls blood pH via H+ and HCO3-
urea
helps form medullary gradient
promotes reabsorption of water
increases concentration of urine
diuretics
chemicals that enhance urinary output (ADH inhibitors, Na+ inhibitors, loop diuretics, osmotic diuretics)
renal clearance
volume of plasma kidneys clear of particular substance in given time
used to determine GFR (detects glomerular damage or follows progress of renal disease)
C=UV/P
chronic renal disease
GFR <60 mL/min for 3 months
in patients w/ DM or hypertension
renal failure
GFR <15 mL/min
causes uremia
treated via hemodialysis or transplant
tubular reabsorption
in PCT
Na+ most abundant
active transport out of cell via Na+-K+ ATPase to peritubular capillaries
passes through apical membrane via secondary active transport or FD
urine
cloudy and increased pH=UTI
yellow pigment from urochrome or urobilin
pink= can indicate blood
brown= can indicate bile pigements
should be clear and pale to deep yellow
pH ranges from 4.5-8.0
ketones and proteins present in urine make it more acidic
95% water, 5% solutes (Na+, K+, PO43-, SO42-, Ca2+, Mg2+, HCO3-)
metabolic wastes= urea, uric acid, creatine
glucose, proteins, ketone bodies, Hb, bile pigments, RBCs, leukocytes should NOT be found in urine
ureter
mucosa= transitional epithelium
muscularis= SM
adventitia= CT
renal calculi
kidney stones in renal pelvis (Ca2+, Mg2+, uric acid salts)
block ureter and cause pressure and pain
can be due to chronic bacterial infection, urine retention, Ca2+ in blood, pH of urine
bladder
stores urine
trigone= smooth triangular area outlined by openings for ureters and urethra; infections tend to persist in this region
mucosa= transitional epithelium
detrusor (smooth muscle)
adventitia= CT
rugae appear when empty
can hold ~500 mL of urine or 2x that amount
urethra
mostly pseudostratified epithelium
internal urethral sphincter= involuntary smooth muscle
external urethral sphincter= voluntary skeletal muscle
micturition
aka urination
1. distention of bladder activates stretch receptors
2. excitation of parasymp neurons in reflex center in sacral region of spinal cord
3. contraction of detrusor by ANS
4. opening of internal urethral sphincter by ANS
5. opening of external urethral sphincter by somatic NS
pontine storage center
inhibits micturition
inhibits parasymp pathways
excites symp. and somatic efferent pathways
pontine micturition center
promotes micturition
excites parasymp pathways
inhibits symp and somatic efferent pathways
incontinence
from weakened pelvic muscles
stress-incontinence= increased intra-abdominal pressure forces urine through external sphincter
overflow incontinence= urine dribbles when bladder overfills
countercurrent multiplier
interaction of filtrate flow in ascending and descending limbs of nephron loops of juxtamedullary nephrons
constant 200 mOsm diff, but is multiplied along the length of loop to 900 mOsm
countercurrent exchanger
BF in ascending and descending limbs of vasa recta
transport solutes and water in two different directions (in and out)
preserve medullary gradient
concentrates urine
renal pyramids
renal medulla
separated into renal columns
renal columns
extension of renal cortex into medulla
tubuloglomerular mechanism
intrinsic control
increased GFR leads to higher concentration of NaCl detected via macula densa cells->constriction of afferent arteriole->decrease GFR
decreased GFR leads to lower concentration of NaCl detected via macula densa cells->dilation of afferent arteriole-> increase GFR
renal pelvis
receives urine from major calyces
layers of surrounding supportive tissue of kidneys
renal fascia
perirenal fat capsule
fibrous capsule
renal arteries
abdominal aorta->renal artery ->segmental arteries->interlobar arteries-> arcuate arteries-> interlobular arteries (cortico radiate)-> afferent arteriole
renal veins
efferent arterioles-> peritubular capillaries->interlobular (cortico radiate) veins->arcuate veins->interlobar veins->renal vein->IVC
nephron loop
employs countercurrent mechanism
ICF
2/3 in cells
40% of body weight
25 L
ECF
1/3 in cells
20% of body weight
plasma= 3 L (20%)
IF= 12 L (80%)
total body water
40 L
water output
must equal input (~2500 mL/day)
60% lost through urine
rest lost via insensible water loss (skin, lungs, perspiration, feces)
osmolality
280-300 mOsm
increase causes thirst and ADH release
decrease causes thirst and ADH inhibition
governed by hypothalamic thirst center and activated via dry mouth, decreased BV and BP, angiotensin II or baroreceptor input, osmolality of 1-2%
decreased ADH
dilute urine
decreased volume of body fluids
increased ADH
concentrated urine
reabsorption of water
increase in volume of body fluids
ADH release
can be triggered by drop in BP, intense sweating, vomiting, diarrhea, severe blood loss, traumatic burns, prolonged fever
hypotonic hydration
cellular overhydration due to rapid excess water ingestion
ECF osmolality decreases (hyponatremia)-> swelling of cells (can cause nausea, vomiting, muscular cramping, cerebral edema, death)
treated via hypertonic saline
dehydration
ECF water loss due to hemorrhage, severe burns, prolonged vomiting, diarrhea, profuse sweating, water deprivation, diuretic abuse, endocrine disturbances
can cause weight loss, fever, mental confusion, hypovolemic shock, loss of electrolytes
edema
accumulation of IF (tissue swelling)
result of fluid out of blood-> can be caused by increased capillary hydrostatic pressure or permeability
can also be caused by decreased fluid going into blood
Na+
controls ECF and water distribution
water in filtrate follows Na+ if ADH present
if lost in urine=water loss
65% reabsorbed in PCT (when H+ are secreted)
25% reclaimed in nephron loops
main ion responsible for maintaining osmotic pressure
K+
affects RMP and muscle cells
increased ECF K+->decreased RMP->delayed repolarization->reduced excitability
decreased ECF K+->hyperpolarization and nonresponsiveness
part of buffer system
acidosis causes increase ECF K+ (H+ moves out, K+ moves in)
alkalosis causes decrease ECF K+ (H+ moves in, K+ moves out)
hypocalcemia
excitability and muscle tetany
hypercalcemia
inhibits neurons and muscle cells
may cause heart arrhythmias
Cl-
major anion in ECF
99% is reabsorbed
maintains osmotic pressure
fewer Cl- reabsorbed when acidosis occurs
anion gap
measured to be 8-12
increased gap can indicate source of metabolic acidosis (keto or lactic acids will replace Cl- instead)
H+
regulated via chemical buffer system, brain stem respiratory centers, renal mechanisms
secreted mostly by PCT
buffer systems
bicarbonate-> only important in ECF buffer; involves H2CO3 and HCO3-
phosphate-> buffer in urine and ICF; involves H2PO4- and HPO42-
protein-> amphoteric; involves COOH and NH4; Hb is a intracellular buffer
alkaline reserve
kidneys replenish bicarbonate via type A cells and ammonium ion secretion
type A cells
generate bicarbonate ions to make blood more basic
type B cells
secrete bicarbonate ions in order to eliminate them and make blood more acidic (reclaims H+)
respiratory alkalosis and acidosis
caused by respiratory failure
most important indicator of blood CO2 levels
metabolic acidosis and alkalosis
indicated by abnormal bicarbonate levels
ammonium ion excretion
more important in acid removal
involves metabolism of gluatamine in PCT (produces 2 ammonium and 2 bicarbonate)
bicarbonate moves to blood and ammonium is excreted in urine
respiratory alkalosis
PCO2 levels <35 mmHg
results from hyperventilation
renal compensation indicated via decreasing bicarbonate levels
due to stress or pain
metabolic acidosis
low blood pH and bicarbonate
due to alcohol poison, persistant diarrhea, ketoacidosis, lacticacidosis, starvation, kidney failure
metabolic alkalosis
high blood pH and bicarbonate
caused by vomiting of acid contents of stomach or excess intake of antacids
respiratory acidosis
renal compensation indicated via high PCO2 and bicarbonate levels
blood pH below 6.8
depression of CNS->coma->death
blood pH above 7.8
excitation of NS->muscle tetany, extreme nervousness, convulsions, death due to respiratory arrest
normal ranges of pH, PCO2, HCO3
pH= 7.35-7.45
PCO2=35-45
HCO3=22-26
decreased pH
due to increased CO2 (what is causing it to be respiratory) or
decreased bicarbonate (what is causing it to be metabolic)
increased pH
due to decreased CO2 (what is causing it to be respiratory) or increased bicarbonate (what is causing it to be metabolic)
venous blood and IF pH
7.35
ICF pH
7.0
increased capillary hydrostatic pressure
can be caused by incompetent venous valves, localized blood vessel blockage, CHF, increased blood volume
increased permeability
can be caused by ongoing inflammatory response
hypoproteinemia
imbalance in colloid osmotic pressure
caused by malnutrition, liver disease, glomerulonephritis
can lead to edema (ascities)
IF
16% of body weight
addison’s disease
adrenal glands do not produce enough cortisol or aldosterone
diabetes insipidus
inability to regulate fluid balance due to deficiency in ADH
