Exam 6- Renal System (without pathology) Flashcards
kidney regulates
- long term blood pressure
- blood cell count /hemoglobin levels (produces erythropoietin)
- Ca2+ homeostasis(activates vit. D)
kidney structure
v
functional unit of the kidney=
nephron
juxtaglom vs cortical neph
m
renal corpuscle=
glomerulus + bowman’s capsule
tubule path
Proximal tubule (convoluted and straight)
Loop of Henle
Distal convoluted tubule
Collecting duct (cortical and medullary)
after collecting duct urine passes to___
minor calyx
major calyx
renal pelvis
ureter
peritubular capilaries surround
cortical segments of tubule
vasa recta surrounds
loop of henle
blood pathways
- efferent arteriole -> peritubular cap-> renal vein
- efferent art. -> vasa recta -> renal vein
three processes involved in urine production
glomerular filtration
tubular resorption
tubular secretion
___+_____+______= amount excreted
amount filtered + amount secreted - amount reabsorbed
filtered load
= “amount filtered”
glomerular filtration barrier needs to achieve=
- high H20 filtration rates
- nonrestricted passage of small/mid sized molecules
- total restriction of serum albumin, proteins and cells
layers of filtration membrane
endothelial cell
basement membrane
pedicels of podocytes/filtration slits with diaphragm
diaphragm between podocytes=
web of nephrin
what is freely filtered trough glom. filtration membrane
water
electrolytes
glucose
amino acids
urea
NOT big protiens and cells
osmolality of plasma and filtrate
300mOsm/kg
[Na+] in plasma and filtrate
both 140mEq/L
[glucose] in plasma and filtrate
100mg/dL
[albumin] in plasma and filtrate
plasma= 4mg/dL
filtrate= NONE
forces that affect filtration
starling forces= hydrostatic pressure oncotic pressure
filtration promoting forces
- Pgc - Glomerular capillary hydrostatic pressure
- π BS- colloid osmotic or oncotic pressure in bowman’s space (but this is practically zero…)
filtration opposing forces
- Pbs- hydrostatic pressure in bowman’s space
- πGC- glomerular capillary oncotic pressure = amount of proteins in plasma
net filtration pressure=
“ultrafiltration pressure” NFP = (+)Pgc - Pbs- πGC
filtration coefficient (Kf) determined by
- hydraulic permeability of the membrane
- surface area of the filtration membrane - both mainly change with disease
glomerular filtration rate =
(equation)
= Kf x NFP = (filtration coefficient) (net filtration pressure)
what makes glomerulus different than other capillary beds
- Kf is very high- lots of fenestrations ~20% of plasma flowing through is filtered
- low resistance in glomerulus, high P in glomerulus
- losing 20% of plasma increase πGC which would oppose filtration, but the high renal blood flow limits this
GFR=____ ml/min or ____L/day
amount of filtrate/min healthy = 125ml/min or 180L/day
healthy people control ___ to ∆ GFR
Pgc
pathologies affect ____ to ∆ GFR
Pbs πGC πBS
___ affect Pgc
Mean arteriole pressure
resistance at afferent and efferent arterioles
MAP decreases = Pgc____ and GFR___
Pgc decreases GFR decreases
afferent arteriole dilates = Pgc____ and GFR___
Pgc increases GFR increases
constrict aff. arteriole = GFR ___
decreases
eff. arteriole dilates = Pgc____ and GFR___
Pgc decreases GFR decreases
constrict aff. arteriole and eff. arteriole at the same time = GFR _____
GFR stays the same
plasma protein concentration increases = πGC____ GFR___
πGC increases GFR decreases
filtration membrane becomes more permeable = πBS____ GFR___
πBS increases GFR increases
kidney stone blocks a ureter = Pbs____ GFR____
Pubs increases GFR decreases
blood flow rates in
kidney cortex=
outer medulla=
inner medulla=
cortex= 4-5
outer medulla= 0.7-1
inner medulla=0.2-0.25
When mean arteriole blood pressure is between ____ the kidney can auto regulate it.
80 to 140mmHg
below range, then GFR is too low
above range, then glomerulus is damaged
two components of auto regulation
- myogenic response
- tubuloglomerular feedback
myogenic response
MAP increases (causes and increased RBF, Pgc, and GFR)
=stretches the afferent arteriole
=afferent arteriole then constricts which then decreases RBF, Pgc, and GFR
tubuloglomerular feedback
increased MAP
=transient increase in GFR
=increase NaCl delivery to macula densa
=release adenosine
=constricts afferent arteriole
small drop in MAP is dealt with by=
myogenic response and tubuloglomerular feedback =dilation of afferent arteriole
HUGE drop in MAP is dealt with by=
myogenic response and tubuloglomerular feedback
=dilates afferent arteriole BUT we’re out of auto regulation range… so our GFR and RBF and Pgc drop… yikes…
autonomic NS responds to HUGE drop in MAP by___
activating SNS = constricts afferent arteriole yikes!!
end results with HUGE decrease in MAP
decrease in perfusion pressure Pgc and GFR
+ autoregulation dilates aff. art.
+ SNS hugely constricts afferent arteriole (further decreasing Pgc and GFR)
=LARGE DECREASE IN PGC AND GFR
why does SNS constrict the aff. arteriole with huge drop in blood pressure
body’s trying to decrease renal blood flow so less blood goes to kidney so it can go to heart and brain
renal artery stenosis
decreased RBF, Pgc, GFR
auto regulatory response to renal artery stenosis
dilate the afferent arteriole AND constricts the efferent arteriole
efferent arteriole is constricted via___
RAAS
- Juxtaglomerular cells =>renin
- (+) angiotensin II which constricts eff. arteriole
NSAIDS effect
inhibits prostaglandins which normally dilate afferent arteriole
decreased effective circulating blood volume (heart failure) causes…
- (+) SNS = constrict afferent arteriole (alpha 1) and (+) B1 on JG to (+) RAAS
- (+) RAAS = constricts efferent arteriole
END RESULT= decreased RBF, but somewhat maintained GFR
large amounts of both NE and Ang II=
decreased RBF, but somewhat maintained GFR
=renal ischemia
=increased prostaglandin production
=dilate the afferent arteriole somewhat counteracts the decrease in RBF and prevents ischemia
why is it bad to take an NSAID if you have heart failure?
NSAIDS (-) prostaglandin aff. arteriole dilation which would increase GFR and RBF and therefore causes lower RBF and GFR which= ACUTE KIDNEY INJURY
Renal Clearance=
Volume of plasma cleared of a substance per unit time Volume/Time
Normal GFR=
125ml/min
A substance is filtered and reabsorbed but not secreted then its clearance is > GFR
LESS THAN
clearance = GFR then _____ reabsorption or secretion
no net
clearance > GFR then there has been net _____
secretion
clearance
reabsorption
p-aminohippurate (PAH)
-not endogenous -at low concentrations PAH is filtered, none is reabsorbed and the rest is secreted ∴ PAH is a measure of renal plasma flow
to measure GFR we need a substance that is ___
freely filtered not reabsorbed not secreted
practically measure GFR via__-
creatinine clearance
creatinine
=endogenous -end product of creatine metabolism -continuously exported to blood by skeletal muscle -freely filtered, not reabsorbed, only a small amount is secreted
ways to measure creatinine
- 24hr urine collection 2. measure creatinine in serum = eGFR (“estimated” GFR)
if your have higher serum creatinine your GFR is
lower than normal, bc you’re not clearing it from the blood
how much urine is produced each day?
1 to 2 L
what is reabsorbed
Water -up to 99%
Good solutes (ie. ions) -majority
Nutrients: glucose, AA - 100%
Urea- maybe half
lipid soluble substances move across epithelial cells interstitial fluid by___ when___
diffusion only when there is a [] gradient
- happens when H2O is reabsorbed urea follows water back into peritubular cap. when H2O is reabsorbed
what is the osmolality of plasma, the filtrate entering the proximal tubule, and the surrounding interstitial fluid?
all the same 300mOsm/kg
who de we get a concentration gradient for water
by resorbing Na+ via mediated transport
mediated transport=
uses energy at some point
draw how glucose is reabsorbed in the proximal tubule
with the reabsorption of glucose what follows____
water via aquaporin-1
movementof ions, glucose and water from interstitial space into peritubular capillary is via___
bulk flow
via starling forces
how much glucose is reabsorbed in the proximal tubule?
all of it
how does glucose end up in diabetic’s urine
the transport maximum of the glucose transporter is exceeded
reabsorption of Na+ accomplishes…
1. reabsorption of solutes
glucose
amino acids
phosphate
water soluble vitamins
Cl- via leaky tight jxns.
2. reabsorption of H2O
3. reabsorption of urea
4. reabsorption of K+ and Ca2+
glucose and amino acids are reabsorbed by primary or secondary active transport in the PCT?
secondary
What is absorbed in PCt
65% of Na+
All the glucose
All the AA
65% of water
transport max of phosphate
lots of Cl-
most HCO3-
50% urea
65% K+
beginig of PCT osmolality=
end of PCT osmolality=
both = 300mOsm/L
what is reabsorbed in the loop of henle
Na+
K+
Ca2+
Mg2+
what parts of the loop of henle are permeable to water
thin descending
-thick and thin ascending are impermeable
thick/thin ascending limb have diffusion/active transport
thin=diffusion
thick =active
draw reabsorption in the thick ascending limb
reabsorption via the Na-K-2Cl cotransporter is considered ____ transport
secondary active transport
efflux of K+ into the lumen and Cl- into the interstitum generates___
a positive transepithelial potential difference
=dirves the paracellurlar transport or resorption of positive ions
___ of NaCl is reabsorbed in loop of henle
20%
osmolality of the filtrate at the beginign and end of loop of henle
begining =300mOsm/L
end=100mOsm/L
we’re resorbing more solute water
=diluting urine
resorption in DCT diagram
what is resorbed in DCT
6%of NaCl
no mo H2O is resorbed and we’re taking out solute so
∴ urine becomes more dilute
osmolality of DCT filtrate at begining and end
begining=100mOSm/L
end=80mOsm/L
draw Collecting duct resorption and secretion
47
aldosterone
function?
draw effects in CD
controls the amount of Na+ resorbed in the CD
loop diuretic inhibits Na-K-2Cl cotransporter in the loop of henle ∴
Na+___
K+___
- more Na+ int he tubule so when it hits the CD they you get more Na+ absorbed in CD
- above causes more K+ secreted = hypokalemia
thiazide diuretic inhibits the Na-Cl cotransporter in DCT
∴ Na+___
K+____
-more Na+ to CD = more Na+ is absorbed
=more K+ secreted= hypokalemia
diuretic inhibits the Na+ channel in the CD
=Na+____
K+___
=decreased Na+ resorptin
=less K+ secreted
= hyper kalemia
draw summary of where Na+ goes in nephron
urine is more/less concentrated than plasm
less
osmolality in different parts of the nephron
slide 4 of 22
ADH function
puts H20 channels on CD
∴ if we want dilurte urine we want low ADH
to prodce a concentrated urine we need:
- CD permeable to H2O
∴ high ADH
- interstitial fluid needs to be concentrated
= a large amout of H2O can be reabsorbed
what makes the interstitial fluid around the CD concentrated?
- countercurrent multiplication
- countercurrent exchange
counter current multiplication
diagram
draw how ADH has effects in the CD
without ADH we would produce ___ urine
dilute
about 50 mOsm/kg H2O
with max ADH we would produce ___ urine
concentrated
about 1200 mOsm/kg H2O
as filtrate goes down CD …
water is reabsorbed, and urine becomes more concentrated
-we can secrete urine anywhere from 50 to 1200 mOsm/kg H1O
extra-cellurlar fluid volume
plasma=3.5L
itnerstitial fluid = 10.5 L
intracellular fluid volume
=28L
blood, interstitial and intracellular concentrations of
Na+
K+
protiens-
H20
diagram
interstitial
H20 in blood increases…
it shifts via osmosis form ECF to ICF to reach equillib
=cell swelling… lysis… death
infuse person with 2L of H2O vs saline
H2O
Osmolality decreases (fatal)
volume of ICF increases
vol. ECF increases
vol. plasma increases
SALINE
Osmolality same
volume of ICF same
vol. ECF increases
vol. plasma increases
a problem wiht osmolality (hyponatremia or hypernatremia) is a ___ problem
water
a ∆ in ECF Na+ changes ___
blood volume and pressure
and NOT the Na+ concentration in the blood
sources of water for the body
drinking
cellular metabolism
how does the body lose water
skin (sweat)
lungs (evap.)
gi (feces)
kidney
what organ regulates water loss
kidney
what stimulates ADH
blood osmolality
osmoreceptors sense increased plasma osmolarity…
- (+) thirst center
- (+) hypothalamic neurons
(+) ADH released from POSTERIOR pituitary
lots of ADH = excrete ___ urine
little ADH = excrete ___ urine
lots of ADH = excrete small vol, concentrated urine
little ADH = excrete lots of dilute urine
___ and ___ are main controllers of total body water and plasma osmolarity
ADH and thirst
central diabetes insipidus
pituitary secretes too little ADH
-from head trauma/tumor/brain surgery
nephrogenic diabetes insipidus
water channel on the nephron doesn’t work
- from genetic mutation or lithium exposure
- ADH levels will be appropriately high
bc blood osmolarity will be high
with a large drop in BP we ___ ADH
increase
so to increase water resorption
(however arteriole constriction has the bigger effect)
what takes presedence volume or osmolarity?
volume
-we will sacrifice osmolarity to increase blood volume
with an high salt meal
total body [Na+] increases
ECF [Na+] stays the same (water shifts out of cells to compensate)
blood volume will be higher
kidney knows total body Na+ is elevated by sensing___
the change in blood volume and pressure
how does kidney regulate Na+ excretion?
- change the GFR to increase Na+ exretion
GFR is highly regulated so maybe not the best way
- Glomerulotubular balance
- RAAS (aldosterone increases Na+ abs. - opp of ANP)
- Atrial Natriuretic Peptide (ANP)
Increaseing GFR’s effect on Na+ excretion=
=(“glomerulotubular balance”)
=more Na+ filtered
=more Na+ reabsorbed in PCT and loop of henle
∴ only 1-2% of extra Na+ is excreted
draw juxtaglomerular apparatus
Juxta glom. senses low Na+
- SNS senses low BP and volume
= (+) JGCs
=>RENIN
- macula densa senses less Na+ in DCT
(+) JGCs
=>RENIN
renin as an enzyme pathway
diagram
what will lower total body Na+ and blood pressure
- raise GFR
- inhibit RAS
- (+) ANP
ANP
when blood volume increases atria stretch
= (+) ANP release
=inhibits Na+ resorption in tubules and increases GFR
what controls K+ balance
- shifting K+ either into or out of cells
- cortical collecting duct
- aldosterone
normal Na+ and K+ levels
Na+ = 135 to 145 mEq/L
K+ =3. 5 to 5 mEq/L
if hyperkalemic
insulin and epinephrine shift into skeletal muscle cell
draw where K is moving in the nephron
draw K+ excretion in CD
draw aldosterone and K+ in CD
Where do we get acids from?
How do we get rid of them?
1. CO2
2. nonvolatile acids
CO2 + H2O ⇔ H2CO3 ⇔ H+ + HCO3-
Metabolism generates CO2
Breathing eliminates CO2
when tissues produce more CO2 blood pH is not altered because…
we increase RR
nonvolatile acids
=any other acid other than CO2 (carbonic acid)
DONT MEMORIZE THIS LIST
=lactic acid
acetoacetic acid
ß-hydorxybutyric acid
phosphoric acid
sulfuric acid
how do we use non volatile acids?
-converted to HCO3-
∴ consumes H+
How does the body deal with this excess acid rom metabolism that generates novolatile acids?
- H+ is buffered by HCO3-, protien or PO3-
- Respiration
- Renal
how fast does the respiratory rate to an increase in nonvolatile acids occur?
quickly … but this fix is limited so we need kidneys
(generally lung responds quickly and kidneys respond slowly)
How does kidney respond to increased H+?
- reabsorption of HCO3- in PCT
- production of new HCO3- in nephron
- coupled ot the excretion of H+
producing a dilute urine is controled more by ___
producing a concentrated urine is controled more by ____
producing a dilute urine is controled more by loop of henle
producing a concentrated urine is controled more by CD
draw two pathways of making new HCO3- in nephron
insert diagram 16 and 17/33
renal response to an increase in non-volatile acids is fast/slow
slow… days
what is respiratory vs. metabolic acidosis or alkylosis?
respiratory= acid base disorder from a mismatch in CO2 production and ventilation
-primary disorder is from a respiratory problem
metabolic= any base distrubance where the primary disorder is not from a respiratory problem
patient has ketoacidosis, but a blood pH test says they’re in normal range… do they still have acidocis
YES
YOU HAVE TO LOOK AT THE WHOLE PICTURE!
-underlying problem is still around even though he’s in a normal range
3 main causes of metabolic acidosis
- diabetic ketoacidosis
(ketone body acids)
- kidney failure
(incresased loss of bicarb, decrease excretion of ammonium and titratable acids)
- diarrhea
(loss of bicarb)
hypoventialation/hyperventilation cause respiratory acidosis/alkalosis
hypo- acidosis
hyper- alkalosis
how does body deal with respiratory acidosis or alkalosis?
kidneys!
resorb or excrete HCO3- and titratible acids
vomiting induced acid-base disorder= metabolic/respiratory acidosis/alkalosis
metabolic alkalosis
-can also be caused by too many antacids…
