Flashcards in Renal Review Deck (138):
Reflection coefficient of <1 means?
membrane is partially permeable to solute. Eventually solute and water will be equal on both sides of membrane
Reflection coeff of 1 means?
Membrane impermeable to solute.
what maintains the gradient of Na and K in cells?
The Na/K ATPase. Na pumped OUT, K pumped IN.
Are Na and K effective osmoles?
YES because every cell has an Na/K ATPase
Blood plasma osmolality determined primarily by what ion?
Na (also glucose, BUN)
what happens if IV KCl is given?
K+ will be taken IN to cells (ATPase) and water will follow in order to maintain osmolarity.
What happens in IV glucose (or D5W) is given?
the volume will be added to ICFV because glucose will be taken up by cells and water will have to follow
what organ produces proteins, which if absent will lead to edema?
liver: without proteins in cells, fluid will to to extracellular/interstitium.
Name 3 ways to increase ICFV
Administer a hypotonic solution
2 ways to increase ECFV
Hypertonic normal saline
one way to increase plasma volume
colloid (with albumin or other proteins that cannot cross membrane)
TBW: breakdown to body water, ICF, ECFV, interstitial fluid, plasma?
BW (water) is 60% of total body weight. ICFV is 2/3 body water. ECFV is 1/3 body water. Interstitial is 3/4 ECFV, plasma is remaining 1/4.
why is the kidney a good sensor of the amount of O2 in blood?
its own O2 usage is proportional to the blood O2 level.
what does the kidney do upon sensing low O2 levels?
upregulates EPO production
Action of angiotensin II on efferent arteriole?
substance to use to measure blood flow through kidney (RBF)?
PAH (because has complete secretion, can be measured in urine)
substance to use to measure clearance filtration rate (GFR)?
inulin. no reabsorption or secretion: perfect measure of FILTRATION. Creatinine is more practical to use though: produced endogenously at constant rate proportional to muscle mass. Will somewhat over-estimate true renal filtration.
What is the range within which GFR and RBF can be autoregulated?
BP of 60 to 180 mmHg
What are 2 mechanisms by which GFR/RBF are autoregulated?
myogenic response (afferent capillary constricts in response to increased pressure in order to protect glomerulus)
tubuloglomerular feedback (increased sodium sensed at macula densa means increased flow rate: feedback constricts constriction of afferent capillaries)
a loop diuretic has what effect on tubuloglomerular feedback?
it eliminates this type of feedback by decreasing the amount of Na brought into cells from the lumen. it therefore increases excretion of urine (since water follows salt)
RAAS system has what effect on BP?
what releases renin? what is the mechanism?
juxtaglomerular cells. when stretched (indication of higher pressure) renin is not released. when relaxed (indicates lower pressure) renin is released.
Describe the RAAS system
Renin catalyzes the reaction of Angiotensinogen -> Angiotensin I. ACE (in lungs) catalyzes AtI -> AtII.
What are the effects of Angiotensin II (4)?
increases Na absorption in prox tubule
constricts efferent arteriole
increases release of aldosterone
Where does aldosterone act? what does it do?
increases Na reabsorption
Increases K excretion
acts in collecting duct
upregulates the mineralocorticoid receptor so the Na/K ATPase is stimulated, and the Na channel on the lumen side is opened wider. effect is more Na in, more K out.
what can compete with aldosterone for the MR receptor in the collecting duct?
cortisol. Cortisol is much more prevalent in the bloodstream than aldosterone and could potentially override aldosterone's control in the collecting duct
what prevents cortisol from binding to the MR receptor in the collecting duct?
11 beta hydroxylase, catalyzes cortisol to cortisone
what inhibits 11-beta-hydroxylase?
licorice, or a gene mutation
what hormones are made in each of the three zones of the kidney?
zona glomerulosa: aldosterone
zona fasiculata: cortisol
zona reticularis: androgens
Where are aldosterone, coritsol, and androgens made?
various zones of the adrenal cortex, which sits atop the kidneys
what is one substance which may increase in concentration along the prox tubule?
xenobiotics: being secreted by kidney
what are the main thing that happen in the prox tubule?
main site of reabsorption of Na, K, phosphate, Ca, H20, glucose, lactate, amino acids. Secretion of xenobiotics.
Prox tubule: urine is concentrated or diluted?
Loop of Henle: urine is concentrated or diluted?
distal tubule: urine is concentrated or diluted?
site of most dilute urine?
end of distal tubule
Describe the osmolar gap. what does it indicate?
osmolar gap is difference between LAB value for plasma osmolality and CALCULATED value for plasma osmolality. Since calculated value only includes Na, BUN, gluc, an osmolar gap indicates presence of something else (often a toxin)
In shock, fluid is drawn from what compartment to what compartment?
From interstitial to plasma (both extracellular)
Isotonic saline will expand what compartment?
the ECFV. reason: if the solution is isotonic, no net movement of water will occur, so the fluid will remain wherever it is initially put
hypotonic saline will expand what compartment?
the intracellular fluid, becasue water will flow from the interstitum inside the cells in order to equalize the osmolarity.
a hypertonic solution will do what to the various compartments?
it will shrink cells
what would be the best way to expand plasma volume with minimal changes to interstitial fluid volume?
a colloid: best would be a whole blood transfusion
does filtration by kidneys require energy? does reabsorption?
filtration: no energy required. reabsorption: energy is required. THUS O2 consumption by kidneys is determined by GFR.
what will happen if you dilate the afferent arteriole? (to RBF, PGC, GFR, FF)
RBF inc, PGC inc, GFR inc, FF inc
what happens if you constrict the afferent arteriole? (to RBF, PGC, GFR, FF)
RBF dec, PGC dec, GFR dec, FF dec
what happens if we dilate the efferent arteriole? (to RBF, PGC, GFR, FF)
RBF inc, PGC dec, GFR dec, FF dec a LOT
what happens if we constrict the efferent arteriole? (to RBF, PGC, GFR, FF)
RBF dec, PGC inc, GFR inc, FF inc A LOT
what is the effect of angiotensin II?
constricts the efferent arteriole
describe the relevant features of podocytes
narrow canals between them, they are very negatively charged
what is the effect of giving NSAIDs to a person with congestive heart failure?
it can lower their GFR considerably
Angiotensin II does what to efferent arteriole?
constricts to maintain GFR
Intrinsic responses to high BP entering kidney?
myogenic response to protect nephron
tubuloglomerular feedback via MD
tubologlomerular balance is what?
2/3 of filtrate is reabsorbed by kidney. consistent proportion.
giving aspirin to someone with heart failure may result in what?
inability to maintain GFR
most of bicarb reabsorbed where?
If bicarb NOT reabsorbed, what might happen?
metabolic acidosis. could be the result of a carbonic anhydrase inhibitor
how does medullary blood flow impact the osmolar gradient between tubule and interstium?
if med blood flow is too fast, may dissapate gradient. want very little flow in most internal part of medulla
how do loop diuretics work?
block the triple transported (Na, Cl, K) in LOH and MD. therefore MD doesn't sense Na load, doesn't feedback to afferent arteriole to constrict (unlike with other diuretics, flow is not diminished to kidney)
aldosterone works where?
How can aldosterone lead to hypo-K?
because it blocks the Na/K exchanger
What can K do directly, and to what hormone?
can directly cause the zona glomerulosa to increase aldo secretion
Hypo and hyper volemia are problems with what?
What system acts to correct hypo andh hyper volemias?
Hypo and hyper natremias are a problem with what?
what system works to solve hypo and hyper natremias?
ADH and aquaporins
What can ADH do if there is a really low BP? why is this not ideal?
if can help solve a low BP issue. Not ideal because it may lead to a low osmolarity issue with plasma. But rather hypo-osmotic than very hypo-volemic
the two hormones of the posterior pitutary?
ADH and oxytosin
what can happen if ADH is blocked?
can become hyper natremic
in central diabetes insipidus, what is the problem? what will serum ADH levels be?
problem is no release of ADH. levels will be LOW
what is the problem with nephrogenic diabetes insipidus? what will serum ADH levels be?
problem is with ADH receptors on kidney. serum levels will be HIGH
what will sense low BP and activate the RAAS system?
cardiac stretch receptors
what are the main transporters (3) in the prox tubule?
Na/H exchanger. blocked by AtII
Na/K ATPase (basalaterol side)
Na/H exchanger with Carbonic Anhydrase. basically a means to reabsorb bicarb
what are the main transporters in the LOH? (1)
Triple transporter: Na, 2Cl, K
what will block the main transporter in the LOH?
what is the main transporter in the MD?
Triple transporter: Na, 2Cl, K
What is the main transporter in the Distal Tubule?
Na/Cl co transporter
what blocks the main transporter in the DT?
What are the main transporters in the CD? (3)
Na channel (driven by Na/K ATPase)
K channel (driven by Na/K ATPase)
What can block the Na and K channels in the CD?
K sparing diuretics
Where is Ca2+ regulated?
What are the 3 actions of PTH?
inc Ca2+ reab from kidney
inc Ca2_ reab from GI tract
pulls Ca2+ out of bones
Exercise: action on K
pulls K out of cells
Insulin: action on K
brings K IN to cells
beta-receptor: epinephrine action on K
brings K in to cells
alpha-receptor: epinephrine action on K
pulls K out of cells
low pH: effect on K
K leaves cells
high pH: effect on K
K enters cells
hyper osmolarity: effect on K
K leaves cells
3 ways diabetes can make you hyper kalemic?
defective insulin (would normally bring in K)
osmolarity (glucose in high conc is effective osmole)
What effect does ADH have on K+ excretion?
no net effect.
3 effects vomiting can have on renal function (generally defined)?
metabolic alkalosis (due to loss of H+ from GI)
hypokalemia (due to nephron exchanging K for H and therefore wasting K)
What are the 2 things that contribute to medullary osmolarity in the medulla?
Na AND urea (600 mOsm each --> 1200 mOsm)
Volume % of RBCs in blood (ie, packed cell volume)
The kidneys regulate the size of the ECFV by regulating the content of what?
How does the body measure volume?
High pressure receptors: Juxtaglom. cells
Low pressure receptors: Cardiac atria, vena cava
Main activities of aldosterone (3)
Via the MR receptor, increases uptake of Na. (in CCD)
inc K excr via increasing Na/K exchange in CCD
inc acid excr.
Normal blood plasma osmolarity value?
Glucose is effective osmole whem?
at HIGH concentrations (>300). Otherwise will be taken in by cell and water will follow
a decr in reflection coefficient will result in what changes to ECFV? interstitial fluid vol? hematocrit?
ECFV: =. Interstitial: inc. hematocrit: incr.
in the thin desc LOH, how much water reabs? how much NaCl?
15% H2O, O% NaCl
Na+ reab in early PT coupled to what luminal protein?
administration of ADH will increase urine osmolarity in what type of diabetes insipidus: central or nephrogenic?
the countercurrent single effect will increase absorption of what by the ascending LOH?
an aldosterone antagonist will do what to ECFV?
a gain of function mutation in the apical Na channel of the CCD will lead to...?
carbonic anhdyrase inhibition will do what to K excretion?
increase K excretion because it will send a big Na load to the CCD, which will exchange Na for K and K waste.
Why do we calc the plasma anion gap?
to see if there is a metabolic acidosis. if the AG is higher than 12, there is a metabolic acidosis.
what does the urine anion gap tell us?
if it's -, the kidney is trying to compensate for a metabolic acidosis by excreting NH4+
How can you tell if a metabolic compensation is for a chronic or acute condition?
the change in HCO3- will be 3 or less for acute, 3 or greater for chronic
If there is a plasma anion gap, what does that indicate about metabolic acidosis v metabolic alkalosis?
indicates metabolic acidosis
How do thiazide diuretics lead to hypercalcemia?
they block Na reabsorption, whicl allows Ca2+ to be transported by calbindin (the Ca2+ taxi!) in distal tubule.
Where is the main site of reabsorption/regulation of Na+?
Where is the main site of reabsorption/regulation of K+
Where is the main site of reabsorption/regulation of PO4-
Where is the main site of reabsorption/regulation of Ca2+
Where is the main site of reabsorption/regulation of H20
acidemia has what effect on plasma Ca2+ conc?
free Ca2+ inc
alkalemia has what effect on free Ca2+ conc?
free Ca2+ dec
What are the 6 hormones of the anterior pituitary?
FLAT P/G: FSH, LH, ACTH, TSH, Prostaglandin, GH
What inhibits the release of GH?
What hormone is constitutively ON unless inhibited?
what inhibits prolactin?
P-OMC polypeptides yield what?
cleaved into a few other polypeptides: ACTH and MSH are most impt
ACTH controls release of what 2 hormones in the adrenal cortex?
cortisol and androgens.
FSH: action in males?
gametogenesis in testis
stimulates sertoli cells to produce androgen binding proteins
FSH: action in females?
promotes follicle growth and estrogen production
LH: actionin males?
promotes testosterone production by Leydig cells
LH: action in females?
stimulates corpus luteum to produce progesterone (maintains a pregnancy) and estrogen
Glucocorticoids: what is the main stimulator for release?
what happens if you have a deficiency of 21-beta hydroxylase?
you will not create aldosterone or cortisol from cholesterol: instead you will create more androgens
How does a dexamethasone suppression test check for the reason for elevated cortisol levels?
check for feedback inhibition: Dex inihibts ACTH and CRH production, so Dex should decr cortisol levels. If it doesn't, there is a way cortisol is being secreted that is external to feedback inhibition. Like a tumor.
A metabolic effect of cortisol?
it is a counter-regulatory hormone; counter effects of insulin. increases blood glucose, promotes hepatic glycogen synthesis, stimulates lipolysis to release FFAs
Describe Addison's disease (primary)
Primary: adrenal cortex is destroyed, cortisol and aldosterone not produced
Addison's disease: secondary
reduced ACTH secr from ant pit -> decr cortisol production
What is the problem with CAH? congenital adrenal hyperplasia?
due to broken enzyme, adrenal cortex is unable to synthesize cortisol and aldo. no negative feedback from cortisol. overproduction of androgens. leads to virilization.
Cortisol and other glucocorticoids bind where?
Addisons crisis involves what?
hypovolemia because you can't stimulate the MR receptor, can't bring in Na in the CCD, can't increase BP. also hyper-pigmentation because MSH is produced along with ACTH (which is upreg'd because no cortisol -> no feedback)