KEY wk 9 lec 2 Flashcards
functional unit of the kidney that filters blood; modify filtrate and turn into urine
nephron
2 parts of nephron
- Glomerulus and
Bowman’s capsule - Uriniferous tubules
2 types of nephrons
cortical nephrons
juxtamedullary nephrons
cortical vs juxtamedullary nephrons
Cortical nephrons – LOH does not descend far into the medulla, no thin ascending LOH
Juxtamedullary nephrons – LOH descends deeply into the medulla, has a thin ascending LOH
function of glomerulus and bowmans capsule
special membrane to form ultra filtrate from blood –> ultrafiltrate into urine
role of proximal convoluted tubule
reabsorb solutes, water, nutrients
waste secretion
role of loop of henle
countercurrent exchangers and multipliers to concentrate filtrate
**concentrate urine
role of distal convoluted tubule and collectiling system
urine composition is finalized via hormones
principal cells: tweak K+, Na+ and water reabsorption/secretion
intercalated cells: pH homeostasis
role of principal and intercalated cells in the distal convulted tubule and collecting system
▪ Principal cells – important in final “tweaking” of K+, Na+ and water reabsorption/secretion
▪ Intercalated cells – important in pH homeostasis
SLIDE 11 chart
kidney primary role
remove substances from bloodstream
via clearance into urine
kidney/ renal clearance
volume of plasma from which a substance is completely removed by the kidneys per unit of time.
kidney’s ability to clear a substance from the bloodstream through urine formation.
removal of substance from blood is expressed in _____. lower blood [ ] means ____ rate of removal
substances from the blood (i.e. meds) is expressed in half-lives – the lower the blood concentration, the lower the rate of removal
3 ways kidney handles substances
- filtration (dissolved substances via starling forces and permeability into bowmans space)
- secretion (transport substances from blood into tubules)
- reasbosrption (transport substances from tubules back to blood)
where does filtration occur in the kidneys? how does it enter and exit? what structures allow for substance to enter?
glomerulus (special capillaries)
via afferent and efferent arteriole
The glomerular capillaries have fenestrations (small pores) that allow for the passage of water, ions, small molecules (such as glucose and amino acids), and waste products from the blood into the Bowman’s capsule, which surrounds the glomerulus.
how much blood is filtered by glomerulus? what cant fit through fenestrations so wont be filtered?
what is the amount of blood available for filtration called? how much of it goes into bowmans space and what is this called?
40%; RBC cant fit so hematocrit isn’t filtered
renal plasma flow
20% of RPF goes into bowmans space = glomerular filtration rate (120ml/min)
whats the GFR
120ml/min
estimated glomerular filtration rate (eGFR)
measure how good kidneys are at filtering waste from blood
the volume of fluid filtered from the kidney’s glomerular capillaries into the Bowman’s capsule per unit time.
what can pass and what cant pass through fenestrations in glomerular capillaries
- small molecules like water, ions, glucose, amino acids, and waste products to pass through
- while retaining larger molecules like proteins and blood cells within the bloodstream.
glomerular filtration barrier permeability based on
size and charge
can slight change surface area and permeability
which ions go through glomerular barrier ? which charge? what cant go through?
sodium (Na+), potassium (K+), chloride (Cl−), and calcium (Ca2+).
The basement membrane and slit diaphragms have a negative charge due to the presence of glycoproteins, which repel negatively charged molecules. This charge barrier helps prevent the filtration of negatively charged proteins, such as albumin, while allowing the passage of smaller ions and neutral molecules.
The glomerular basement membrane and the slit diaphragms are more permeable to
smaller, more positively- charged solutes
but if small, i.e Cl- can go through
starling forces
hydrostatic pressure driving water OUT of a capillary and oncotic pressure pulling water INTO a capillary
what determines GFR
net filtration pressure (i.e. via starling forces and leakiness) and blood flow
what is the main regulator of GFR
arteriole tone of afferent and efferent arteriole
afferent and efferent arteriole role in GFR
afferent is before glomerus (filter system) and efferent is after
- Afferent arteriole:
▪ Constrict: decreases
GFR
▪ Dilate: increases GFR
▪ Impacts delivery of blood to the capillary (changes PGC) - Efferent arteriole:
▪ Constrict: increases
GFR
▪ Dilate: decreases GFR
▪ Constriction causes blood to “back up” in the capillary, increasing
PGC
as fluid moves along the length of the capillary, the net filtration pressure decreases… why might this be?
oncotic pressure rises and hydrostatic pressure slightly falls,
more of the concentrated stuff inside than out; more pressure inside (Oncotic) so then the net filtration pressure decerases bc you already have lots inside??
how does glomerulus maintain constant GFR despite changes in blood pressure
autoregulation
what is auto regulation in GFR
what 2 mechanisms
myogenic response (contraction and relaxation of smooth muscle cells in the afferent arteriole in response to changes in blood pressure)
tubuloglomerular feedback (feedback from the tubules to the glomerulus to regulate filtration) the macula densa feeds back on the GFR based on Na+ (NaCl)
neuro-hormonal regulation of GFR
RAAS
SNS
myogenic response for auto regulation in GFR
pressure in afferent arteriole increase cause the arteriole to ______
as pressures in the afferent arteriole increase, the arteriole contracts –> modest reduction of blood flow into the glomerulus
tubuloglomerular feedback in the GFR
what things at the juxtaglomerular apparatus affect this?
tubules “read” the filtrate and feed back onto the glomerulus, altering filtration rate
▪ Macula densa
▪ Granular cells (secrete renin)
▪ Extraglomerular mesangial cells
auto regulation- TGF
what happens if too much solute (NaCl) to the macula densa
-macula dense released ATP or adenosine
-less renin secreted by granular cells
-angiotensin II decreases
-less dilation of afferent, less constriction of efferent arterioles
-GFR drops
CHART ON SLIDE 37
:)
auto regulation- TGF
what happens if too little solute (NaCl) to the macula densa
-prostaglandins are released by macula densa
- increase renin; vasodilate afferent arteriole
-prostaglandins prevent excessive constriction that would be done via angiotensin II (fine tune arteriole tone)
macula densa releases what when too much solute vs too little solute
too much: ATP, adenosine
too little: prostaglandins
if too much that leads to decrease renin, angiotensin II and GFR
what does macula densa release if theres an increase in tubular flow but the solutes arent to little or too much
release nitric oxide (blunt reduction in GFR)
angiotensin II impacts on GFR and arterioles
constricts afferent a bit, but efferent a lot –> increase GFR, increase renal resistance, increase reabsorption of fluid at tubules
how is angiotensin II released in GFR
tubuloglomerular feedback (TGF) and baroreptor of granular cell of JGA (when afferent arteriole pressure drops, granular cells release more renin)
epinephrine impacts on GFR
constrict afferent and efferent arterioles (SNS)
decreases renal blood flow (RBF) and GFR
*released when serious ECF depletion
norepinephrine impact on GFR
increase renin release from granular cells
which increases angiotensin II and increases GFR
epinephrine vs norepinephrine impacts on GFR
epi: decrease RBF and GFR (constricts both afferent and efferent)
NE: increases renin; increase ATII; constrict afferent a little, constrict efferent a lot; increase GFR
endothelin impact on GFR
what causes its release?
vasoconstrict; reduce blood flow to nephron and reduced GFR
released by damaged vascular endothelial cells of kidneys
natriuretic peptide (ANP, BNP) impact on GFR
released via heart (atria) from volume overload
inhibit renin; relax afferent arteriole; increase GFR
relax intraglomerular mesengial cells; increase surface area for filtration
increase GFR and fluid excretion
azotemia
low filtration at glomerulus (build up of waste in the blood)
3 types of azotmeia (low filtration at glomerulus)
pre-renal azotemia
renal azotemia
post renal azotemia
pre-renal azotemia
causes and problem
(Low Blood Flow to Kidneys)
- Causes: Dehydration, shock (hypovolemic/cardiogenic), heart failure (CHF), arteriole dysfunction.
- Problem: Kidneys aren’t getting enough blood to filter.
renal azotemia
causes and problem
(Kidney Damage)
- Due to glomerular or tubular damage (specific causes discussed later).
- Problem: Kidneys are damaged and can’t filter properly.
post-renal azotemia
causes and problem
(Urine Flow Blockage)
- Blockage in both ureters or bladder/urethra prevents urine from leaving.
- Problem: Backpressure reduces filtration.
substances that only get filtered by glomerulus
inulin
creatinine
inulin in the kidneys
only filtered, not secreted or reabsorbed
use to measure GFR via IV injection and get it to steady state in bloodstream
creatinine in GFR
released at constant rate by many cells. mainly filtered, only secreted a very small amount
steady state between production and clearance
measure clearance of creatinine via
[Cr]blood, urine flow rate, [Cr]urine
blood sample + 24 hour urine
measure GFR via
inulin or cystatin C
cystatin C is made at steady state in body and less prone to error than creatinine
glucose clearance measurement
is 0: it is filtered and completely reabsorbed bc need it for energy
if glucose in urine could be diabetes bc glucose transporters are fully saturated or blocked
parts of filtration barrier in glomerulus
- Fenestrations in glomerular capillaries
- Basement membrane
- Spaces between the pedicels of podocytes (filtration slits)
