Unit 4 - Renal Physiology Flashcards
Where are Glucose carriers located in a nephron?
proximal collecting tubule
transepithelial transport
5 barriers to being reabsorbed:
- luminal membrane of tubular cell
- pass through cytosol to get to other side of cell
- cross basolateral membrane of tubular cell to interstitial fluid
- diffuse through interstitial fluid
- penetrate capillary wall to enter blood
juxtaglomerular apparatus
macula densa cells: part of tubule
- monitor & respond to changes in osmolarity of filtrate
granular cells: modified smooth muscle of afferent arteriole
- serve as baroreceptors sensitive to blood pressure
mesangial cells: contain contractile elements
Three forces that influence glomerular filtration
- glomerular capillary blood pressure - favors filtration
- plasma colloid osmotic pressure - opposes filtration (exerted by plasma proteins)
- Bowman’s capsule hydrostatic pressure - opposes filtration
what is filtered load?
the quantity of any substance filtered per minute (mg/min)
FL = plasma concentration X GFR of substance
define tubular maximum (aka transport maximum)
the maximum reabsorption of a substance. Any quantity filtered beyond it tubular maximum, is not reabsorbed & will show up in urine.
Renin-Angiotensin-Aldosterone system (TAAS)
- promotes salt and water retention
- leads to a rise in arterial blood pressure
granular cells
- part of the juxtaglomerular apparatus
- respond to:
- fall in NaCl
- ECF volume
- arterial blood pressure - if falls, secrete renin - secrete RENIN
Renin
- activates ANGIOTENSINOGEN to become ANGIOTENSIN I.
- brings about increased Na+ reabsorption in distal & collecting tubules
angiotensinogen
- plasma protein synthesized by LIVER
- present in plasma
- secretion of RENIN activates it to become ANGIOTENSIN I
Angiontensin I
- when passing through lungs, it’s converted to ANGIOTENSIN II by ANGIOTENSIN-CONVERTING ENZYME (ACE)
Angiotensin II
- tells adrenal cortex to secrete ALDOSTERONE
- increases TPR by constricting systemic arterioles
- stimulates thirst
- stimulates vasopressin
Aldosterone
increases Na+ reabsorption by:
- inserting add’l Na+ channels into luminal membranes
- adding Na+-K+ pumps into basolateral membranes
promotes Na+ reabsorption & K+ secretion
hypoventilation would lead to:
respiratory acidosis
in which case is the pH lower: hypo ventilating or hyperventilating
after hypo ventilating = respiratory acidosis
body’s response to metabolic alkalosis
body retains more carbon dioxide
3 components of filtration membrane
- capillary endothelium
- basement membrane
- filtration slits of podocytes
which part of the tubule is always impermeable to water?
ascending limb
a decrease in concentration of plasma proteins will _______ filtration pressure?
increase
How will auto regulation respond to a drop in GFR?
dilation of afferent arteriole to increase blood flow & glomerular pressure
What would loss of plasma proteins do to GFR?
will decrease oncotic pressure (works against filtration) -> GFR would increase
What would dehydrating diarrhea do to GFR?
would increase oncotic pressure -> GFR decrease
Autoregulation of GFR
Happens in the kidneys; regulate between 80 - 180 mmHg MAP
- myogenic: adjust diameter of afferent arteriole
- tubuloglomerular feedback:
Autoregulation of GFR: tubuloglomerular feedback for Low GFR
detect changes in NaCl concentration
1. for low salt (to increase GFR): macula densa detect low salt; intrarenal baroreceptors -> granular cells to release RENIN - > increased Na+ reabsorption -> increased water retention -> increased BP -> increased GFR
Autoregulation of GFR: tubuloglomerular feedback for high GFR
high salt concentration (to lower GFR): macula densa cells detect high salt -> release ATP & adenosine -> cause granular cells to constrict afferent arteriole -> lower GFR
GFR Regulation - 3 pathways
All control afferent arteriole diameter & extrinsic overrides intrinsic
Intrinsic control
1. autoregulation
Extrinsic control - make adjustments to BP which affects GFR
- Neural regulation
- Hormonal control
GFR regulation: Extrinsic: Neural reg
- sympathetic control - if stimulated b/c too low, causes a system wide constriction of arterioles, which increases BP and therefore GFR
if too high - sympathetic activity is reduced
- baroreceptor reflex - baroreceptors in aortic arch & carotid sinus detect low BP; triggers RAAS, which increases BP and GFR
GFR reg / extrinsic / neural regulation
- sympathetic control
2. baroreceptor reflex
GFR reg / extrinsic / hormonal regulation
- Angiotensin II - increase BP
2. ANP - atrial natriuretic peptide - decrease BP
renal threshold
the plasma concentration at which transport maximum is reached
substance will begin to appear in urine
obligatory reabsorption occurs where?
Refers to H20 reabsorption done osmotically
80% done this way
1. proximal collecting tubule (PCT)
2. Loop of Henle
facultative reabsorption occurs where?
Water reabsorption that requires ADH to be present
20% done this way
1. distal collecting tubule (DCT)
2. collecting ducts
This step determines whether grin will be concentrated or diluted
Countercurrent Multiplier
- establishes the gradient - juxtamedullary nephron
- preserves the gradient - vasa recta
- uses the gradient - DCT, collecting tubules
micturition
voiding bladder or urination
a spinal reflex
internal sphincter: smooth muscle; contracts
external sphincter: skeletal; relaxes
ADH
released from posterior pituitary
osmoreceptors in kidneys & hypothalamus dectect osmotic changes
ph of blood
7.35 - 7.45
< 7.35 = acidosis - depression of CNS
> 7.45 = alkalosis - over excitability of nervous system
Mechanisms for Acid-Base Balance in body
- Chemical buffer systems
- Respiratory buffer systems
- Renal mechanisms
Chemical buffer systems
Should resist changes in H+ concentrations
- bicarbonate: H2CO3 / HCO3-
- phosphate: NaH2PO4 / Na2HPO4
- protein buffer : Hb
respiratory acidosis
too much CO2 / hypoventilation to fix: buffer: take up H+ no respir renal: excrete more H+, conserve HCO3-
respiratory alkalosis
not enough CO2 / hyperventilation to fix: buffer: give up more H+ respir: restrict hypervent renal: conserve H+, excrete more HCO3-
metabolic acidosis
caused by HCO3- deficit / severe diarrhea, diabetes mellitus
to fix:
buffer: take up H+
respir: blow off add’l H+ generating CO2
renal: excrete more H+, conserve HCO3- (except w/kidney disease)
metabolic alkalosis
caused by excess HCO3- / prolonged diarrhea, ingestion of too many antacids to fix: buffer: liberate more H+ respir: hyperventilation restricted renal: conserve H+, excrete more HCO3-
