Renal Physiology Flashcards
movement of particles across membranes is driven by this
gradients
Lipid bilayer prevents movement of what two kinds of molecules
charged (Na+, K+, Mg++, Ca++) Polar molecules (glucose)
Lipid bilayer allows crossing of what two kinds of molecules
Lipid soluble (antidiuretic, aldosterone) Small polar (H2O
Diffusion
movement of particles from high to low passively across the membrane without a transporter
Facilitated diffusion
“money maker”
moves particles from low to high across the membrane with a transporter
particles cannot cross without the transporter
two factors affect the rate of diffusion and facilitated diffusion
size of the gradient (larger = faster)
permeability of the membrane to the solute (more permeable/more pores = faster)
active transport
movement from low to high concentration, against electrochemical gradient requires ATP (converted to ADP by hydrolysis)
secondary active transport
movement from low to high concentration, against electrochemical gradient
requires potential energy generated by an active transporter
symport
cotransport in the same direction
facilitated by symporter
antiport
cotransport in opposite directions
facilitated by antiporter
osmosis
movement across a selectively permeable membrane
effective osmole
molecule will not cross the membrane, creates a concentration gradient
ineffective osmole
molecule will cross the membrane and will not create a concentration gradient
osmolarity
concentration of osmotically active things in a solution
Tonicity
concentration of effective osmoles (things that cause osmosis)
three types of tonicity
hypotonic: low effective osmolarity
hypertonic: high effective osmolarity
isotonic: same effective osmolarity
Gross morphology from exterior to interior
capsule, cortex, medulla, pyramid (base, apex, papillae), renal pelvis, hilus
contents of the nephron in the cortex
Renal corpuscle, proximal convoluted tubule, proximal straight tubule, some distal straight and distal convoluted
contents of the nephron in the medulla
loop of Henle, collecting ducts, some distal straight and distal convoluted tubule
what structures make up the renal corpuscle
afferent arteriole, macula densa, glomerulus (podocytes and pedicles), Bowman’s capsule, efferent arteriole
features of the efferent arteriole that increases the blood pressure in the glomerulus
small diameter, less stretchy
what components of podocytes/pedicles contribute to filtration apparatus in the glomerulus
walls of capillary, basement membrane (lamina rara interna, lamina densa, lamina rara externa), slit diaphragm
components of the proximal tubule that differentiate it’s function
microvili and apical canaliculi (increases surface area for absortpion)
lots of mitochondria (uses lots of ATP)
loop of Henle absorption
descending limb: H2O and Na/Cl
ascending limb: Na/Cl only
hormone that enables distal part of distal tubule to be permeable to water
antidiuretic hormone
three parts of juxtaglomerular apparatus and theyre function
macula densa: direct contact with the filtrate
extraglomerular: recieve info from macula densa
juxtaglomerular: secrete renin, angiotensin converting enzymes and angiotensin 1&2
principal cells function and location
reabsorption, cortical collecting tubule, inner&outer medullary collecting tubule, papillary collecting tubules
intercalated cells function and location
secretion (H, HCO3), cortical collecting tubule, outer medullary collecting tubule
glomerular filtration barriers
size: pores with different sizes to exclude large molecules
Charge: negatively (anionic) charged proteins in the glycocalyx
starling’s forces out of the capillary
capillary hydrostatic pressure (Pc) and Bowman’s space oncotic pressure (πbs)
starling’s forces into the capillary
bowmans space hydrostatic pressure (Pbs) and Capillary oncotic pressure (πc)
constricting/relaxing afferent and efferent arterioles affect on GFR
constrict: decrease GFR, decrease Pc
relax: increase GFR, increase Pc
heartworm and lyme disease affect on GFR
produces antigens that get stuck in the glomerulus
plasma protein changes affect on GFR
affects πc
increase protein: decrease GFR
decrease protein: increase GFR
obstructions in urinary system affect on GFR
affects Pbs
increase Pbs: decrease GFR
decrease Pbs: increase GFR
autoregulation
the range of blood pressures where the kidney is able to maintain filtration rate independent of systemic blood flow
myogenic autoregulation
preventative autoregulation
vasoconstriction (at high blood pressure) and vasodilation (at low blood pressure) in the afferent arteriole
tubuloglomerular feedback
regulatory autoregulation by sensing ultrafiltrate ionic constituents, signaling parts of juxtaglomerular aparatus and stimulating autoregulation
NKCC2
part of macula densa cells, senses Na, K, Cl concentration in ultrafiltrate
release of ATP/adenosine in tubuloglomerular feedback, where and what it does
released from macula densa, activates extraglomerular mesangial cell receptors
extraglomerular mesengial cell function in tubuloglomerular feedback
receives ATP/adenosine signal from macula densa
increases Ca to contract afferent arteriole
inhibits release of renin from juxtaglomerular cells
angiotensinogen
produced in liver, interacts with renin to become angiotensin 1
angiotensin 1
interacts with angiotensin converting enzyme in the lung, becomes angiotensin 2
functions of angiotensin 2 in high blood pressure
systemic arteriolar vasoconstriction (increases blood pressure)
stimulates antidiuretic secretion and thirst
increases tubular uptake of NaCl
functions of angiotensin 2 in low blood pressure
systemic vasoconstriction (especially on efferent arteriole)
increases PGE2 release from macula densa
stops renin release
release of PGE2 during low blood pressure juxtaglomerular feedback
released by macula densa
stimulates afferent arteriole vasodilation
stimulates juxtaglomerular to release renin - increases angiotensin 2
3 important facts about the Na/K ATPase
3Na out for 2K in
requires ATP
maintains the electrochemical gradient (with low intracellular Na)
things the proximal tubule reabsorbs
water, Na, solutes, glucose, amino acids, bicarb
things the proximal tubule secretes into tubular fluid
H, anions
ways Cl is absorbed
Cl/anion antiporter (with electrochemical gradient) Paracellular diffusion (will bring Na across too)
protein reabsorption
occurs in proximal tubule
partially degraded on luminal membrane, fully degraded by lysosomes, amino acids absorbed on basolateral membrane
Loop of Henle ascending limb reabsorption
NaCl (25%)
passive
Loop of Henle descending limb reabsorption
H2O (15%)
passive
NKCC1 symporter
brings Na, K, 2Cl into the cell
K is against concentration gradient
loop diuretics
inhibit the work of the NKCC1 symporter
thiazide diuretics
inhibit the work of the Na/Cl symporter
antidiuretic hormone affect on distal tubule
enables water reabsorption, the cells are otherwise impermeable to water
Principal cells in collecting ducts reabsorb what
NaCl and H2O if antidiuretic hormone is present
channels in principal cells are sensitive to what
Na channels: amiloride
aquaporins: antidiuretic hormone
Principal cell K homeostasis
K leaves down gradient into tubular fluid and interstium via passive channels
purpose of intercalated cells and active enzyme
maintain acid base balance
carbonic anhydrase
concurrent multiplication
two factors create the idea environment for the reabsorption of Na and H2O in the loop of henle
descending limb concurrent multiplication
permeable to H2O, moves passively out because Na osmolarity is higher in interstitium as the loop descends
hairpin loop concurrent multiplication
tubular fluid osmolarity = interstitium osmolarity BUT Na is more concentrated in tubular fluid
Ascending loop concurrent multiplication
Na passively moves out by the concentration gradient until the distal tubule
distal tubule role in concurrent multiplication
active transport of Na into interstitium, creates osmolarity for H2O to leave the tubular fluid
antidiuretic hormone function
regulate water conservation
no/low is water expelled in the kidney
high is conserved water (reabsorbed into the blood)
antidiuretic hormone stimulus and location
Released from anterior pituitary
release stimulated by high extracellular osmolarity (osmoreceptors in hypothalamus)
release stimulated by low extracellular volume (baroreceptors in coronary sinus and aorta)
antidiuretic hormone function on urea
high concentration stimulates medullary collecting duct permeability, allowing urea into interstitial fluid
urea function on reabsorbtion
effective osmole in tubular fluid in loop of Henle (helps absorb H2O in the descending limb)
ineffective osmole in collecting duct
Vasa recta
hairpin loop of capillaries throughout the kidney
Vasa recta goal
removes water from interstitium back into circulation
keeps Na in interstitium
works because there are no permeability differences in the capillary
determinant of extracellular osmolarity
concentration of Na in extracellular fluid
determinant of extracellular volume
amount of sodium in extracellular fluid
hypernatremia and signs
high osmolarity of Na in extracellular fluid
water moves out of cells
cerebral vessel hemorrhage, muscle weakness, neurological signs, coma
hyponatremia and signs
low osmolarity of extracellular fluid
water moves into cells
cerebral and pulmonary edema, muscle weakness, incoordination, seizures
osmoreceptors
senses ECF osmolarity
High ECF osmolarity increases ADH, increases thirst
decreases Na in blood
hypervolemia and signs
increased extracellular volume, ascites and pulmonary edema
hypovolemia and signs
decreased volume, organ damage (from O2 depletion) low blood pressure, tachycardia
baroreceptors
senses ECF volume
High releases natriuretic peptide, stops ADH, decreases blood volume
Low stimulates ADH and sympathetic nervous system, increases blood volume
Juxtaglomerular appartus role in ECF volume
senses low ECF and stimulates renin-angeotensin system
sympathetic flow
increases Na and H2O reabsorption, increasing ECF volume
releases norepinephrine
stimulates transporters in proximal tubule
stimulates renin release
norepinephrine
vasoconstrictor, increases glomerular filtration rate
increases Starling’s forces on Na reabsorption at peritubular capillaries
Starling’s forces changes because of decreased ECF
higher tubular hydrostatic force (because higher golmerular filtration rate) pushes fluid out of tubules
Capillary hydrostatic pressure decreases, capillary oncotic pressure increases - both cause Na and H2O to be reabsorbed into the capillary
Angiotensin II effect on low ECF
Increases Na/H2O uptake into capillary Constricts efferent arterioles stimulates Na/H antiporter in proximal and distal tubules Stimulates ADH release Stimulates aldosteron
Aldosterone
increases Na uptake
increases Na/K ATPase
increases NKCC1
increases permeability of Na channels in collecting duct
Natriuretic peptides goal
responds to hypervolemia
promotes Na excretion, reduces H2O reabsorption, decreases ECF
Natriuretic peptide function
constricts efferent arteriole, dilates afferent arteriole
inhibits renin-angiotensin system (renin, ADH, Aldosterone)
inhibits Na channels - NaCl reabsorption in collecting ducts
