Kidney Flashcards
What structures are found in the renal medulla?
loops of henle and collecting ducts
what is found in the renal cortex?
everything else that makes up the nephron
the pyramids are part of the renal cortex or medulla?
medulla
which two organs are the primary regulators of acid base balance? which acids do they excrete?
kindeys (excrete non volatile acids)
lungs (excrete volatile acids CO2)
decreased O2 delivery to the kidneys has what effect on EPO production?
increased EPO production
severe kidney dz has what effects on EPO production leading to what?
decreased EPO production leading to anemia
what hormones are produced by the kidneys?
EPO
calcitrol (active Vit D)
prostaglandins
low blood Ca has what effect on PTH levels?
low blood Ca causes an increase in PTH
increased PTH does what to calcitriol?
^PTH>^Calcitriol (active Vit D)
what does aldosterone cause? what does it primarily control?
Na and H20 reabsorption and K and H excretion.
primarily controls extracellular fluid volume
what does ADH do and what does it primarily control?
only H20 reabsorption. so it primarily controls plasma oxmolarity
long term BP control mechanism?
thirst and Na / H20 excretion
intermediate BP control
RAAS
where is renin produced?
JGA cells
where is aldosterone produced?
adrenal cortex
short term BP control?
baroreceptor reflex
what to know about phase 1 and phase 2 reactions in regards to the kidney and liver?
both the kidney and liver can do phase 1 and phase 2 biotransformation reactions
what does EPO cause?
stem cells in the bone marrow to produce more RBCs
what prostaglandins are produced by the kindeys and what is their function?
PGE2 & PGI2 vasodilate renal arteries
Thromboxane A2 constricts renal arteries
what are the three effects of increased serum calcitriol levels?
- ^ intestinal Ca absoprtion
- decreased Renal Ca and phosphate excretion
- ^ deposition of Ca into bones and ^ resorption of old bone. (this just helps turn bone over)
remember: calcitriol levles raise serum Ca levels.
increasing serum Ca levels has what effect on PTH levels?
as Ca increases PTH decreases
can the kidneys create glucose?
yes, can sythesize glucose from amino acids like the liver.
do the kindeys or the liver make more gluocse?
Kidney’s rival the livers ability to perform gluconeogenesis.
Kidneys get what percent of CO?
20-25%
how is renal blood flow divided?
90% goes to cortex and 10% goes to renal medulla and juxtamedullary nephrons
what is the average PaO2 in the renal cortex vs renal medulla? why is this importnat?
PaO2 is about 50 in renal cortex and only 10 in renal medulla. This is why renal medulla and juxtamedullary nephrons are so sensitive to ischemia
how much blood is filtered at the glomerulus?
about 20%
what happens to the other 80% of blood that is not filtered through the glomerulus?
just circulates through the peritubular capillaries
how much of the ultrafiltrate is reabsorbed into the peritubular capillaries?
99%
how much urine is produced each day?
about 1-1.5L urine excreted each day
how much does renal blood flow decrease for each decade of life after age 50?
decrease by 10% for each decade after 50yrs
explain renal blood flow ammount in a neonate
RBG doubles in the first 2 weeks of life, and reaches acult levels by age 2yr.
RBF is autoregulated in what range?
texts varry widely, but apex likes MAP 50-180
is urine output autoregulated?
No, it is linearly related to MAP > 50
what are the two most important mechanims for renal autoregulation?
myogenic mechanisms and tubuloglomerular feedback
explain the myogenic mechanism of renal autoregulation?
increased renal artery pressure > afferent arteriole constriction to protect glomerulus from excessive pressure.
decreased renal artery perfusion > afferent arteriole dilation to increase blood flow to nephron
describe tubuloglomerular feedback mechanism of renal autoregulation
JGA is in the distal tubule between afferent and efferent arterioles.
Na and Cl concentrations in the distal tubule affect afferent arteriolar tone
explain nervous system innervation of the kidney
very limited PNS innervation
SNS innervation of the afferent and efferent arterioles. This typically overridden by internal autoregulation. However, during extreme stress or excessive catecholamines SNS can cause decreased renal blood flow.
explain the surgical stress response effects on the kidneys
surgical stress an cause transient state of vasoconstriction and Na retention for up to several days which leads to oliguria and edema, predisposing the kidney to ischemic injury and effects of nephrotoxic drugs.
Where is the JGA located?
in distal tubule between afferent and efferent arterioles
explain the effect of decreased RBF on the JGA
decreased RBF > decreased GFR > decreased Na and Cl delivery to to JGA (sensed by the macula densa) > dilation of afferent arterioles to ^ GFR
how do low Cl levles in ultrafiltrate affect the JGA cells?
low Cl levels in ultrafiltrate > Renin release from JGA cells > RAAS activation. RAAS activation > efferent arteriole constriction which also ^ GFR.
what three systems control BP?
SNS
RAAS
Vasopression system
what triggers RAAS?
decreased renal perfusion
where is angiotensionogen made?
the liver
explain steps of RAAS
Renin converts angiotensinogen to angiotension 1
ACE in the lungs converts angiotension 1 to angiotension 2
angiogensin 2 has 5 effects
what else does ACE do besides convert angiotensin 1 to angiotensin 2?
also breaks down brandykinin into inactive proteins.
increased bradykinin from ACE inhibitors can cause what sysmptoms?
cough
allergy symptoms
angioedema
bronchospasm
what are the 5 effects of angiotensin 2
vasoconsctriction (very potent)
^ aldosterone
SNS activation
^ ADH
^ Thirst
What 3 things increase Renin release and give examples of each
- Decreased Renal perfusion (hemorrhage, PEEP, CHF, liver failure with ascities, sepsis, diuresis)
- B1 / SNS activation
- Tubuloglomerulur feedback ( decreased Na or Cl in distal tubule)
effects of aldosterone and mech of action
Na and H2O retention with K and H excretion.
this happens via Na/K ATPase in principal cells of distal tubule and collecting ducts
what three things increase aldosterone release?
RAAS
hyperkalemia
hyponatremia
sodium retaining effects of angiotension 2 happen how quickly?
almost immediately
how soon do physiologic effects of aldosterone kick in after aldosterone release?
1-2hr delay between release and physiologic effects
what is Conns disease? What does it cause?
excess aldosterone. Leads to Na retention and K loss
when do we see inadequete aldosterone release?
very rare to seee inadequete aldosterone in isolation
most commonly seen as a result of addisions disease or adrenocortical insufficiency.
what is addisions disease?
usually the result of adrenocortical insufficiency.
Inadequate production of adrenal hormones, mainly cortisol and aldosterone.
what is normal plasma osmolarity?
280-290mOsm/L
what is the main determinant of plasma osmolarity?
Na concentration
what is the formula to calculate plasma osmolarity?
plasma osmolarity = 2Na + glucose/18 + BUN/2.8
another name for ADH
arginine vasopressin or vasopressin
what two things increase ADH release?
^ osmolarity of ECT
decreased blood volume
ADH mech of action
- V1 receptors cause peripheral vasoconstriction
- V2 receptors cause ^ H20 reabsorption (increased aquaporin channels inserted into the wall of the collecting ducts)
ADH half life
5-15min
where is ADH systhesized?
primarily in the supraoptic nuclei of the hypothalamus, but small amount is also synthesized in the paraventricular nuclei.
what are the three pathways of renal vasodilation?
- prostaglandins
- naturetic peptides
- Dopamine receptors
pathophys of renal vasodilation from prostaglandins
leukotrines cause vasoconstriction
when hypoxic pathway goes to vasoconstrictors from cyclic endoperoxides instead of the other way
what 4 things can increase phospholipase A2 leading to renal vasodilation?
ischemia
hypotension
NorEpi
angiotensin 2
Basically the stress response will triggers events that are designed to preserve renal blood flow
how do NSAIDs affect renal vasodilation pathway from prostaglandins
inhibit cycloxygenase resulting in renal vasoconstriction
describe pathophys of naturetic peptide pathway for renal vasodilation
ANP > inhibits renin release > causes vasodilation, Ha and H2O excretion in the collecting ducts
name the dopamine receptors and their location
DA1 in renal vasculature and tubules
DA2 in pre-synaptic SNS nerve terminals
list the function of DA1 and DA2 receptors
DA1 ^ cAMP > vasodilation, ^ RBF, ^ GFR, diuresis, and Na excretion
DA2 decrease cAMP > decreased NorEpi release
how does renal dose dopamine effect the kidneys?
dopamine does increase Urine output, but no solid evidence supports dopamine as a treatment or prevention of AKI
Fenoldopam med class
selective DA1 receptor agonist
Fenoldopam effects
^ RBF
Fenoldopam dose and effects
0.1-0.2 mcg/kg/min ^ RBF, ^GFR, ^ Na excretion with no effect on arterial BP
during which surgeries does fenoldopam offer renal protection? when does it affect mortality rates?
aortic surgery and CPB
also decreases the need for dialysis and in-hospital mortality in cardiac surgery patients.
what is the normal glomerular filtration rate?
125ml/min
what percent of renal blood flow is filtered through the glomerulus? What percent is delivered straight to the peritubular capillaries
20% filtered through glomerulus
80% delivered to peritubular capillaries
what substances are freely filtered at the glomerulus and what substances are not?
H20, electrolytes, and glucose are freely filtered
plasma proteins are not filtered
when can plasma proteins enter the tubules?
in kidney disease the basement membrane is destroyed which allows proteins to enter the tubules and can lead to hypoalbuminemia
two examples of kidney disease where proteins are lost in the urine
nephrotic syndrome
interstitial nephritis
what is the main determinant of GFR?
glomerular hydrostatic pressure
what are the 3 determinants of glomerular hydrostatic pressure
- Arterial BP
- Afferent arteriole resistance
- Efferent arteriole resistance
how do increased and decreased plasma protein concentration affect GFR and filtration fraction?
increased plasma proteins > decreased GFR, and decreased filtration fraction
decreased plasma proteins > ^ GFR and ^ filtration fraction
explain the affects of efferent arteriole constrction on RBF and GFR
biphasic pattern
mild constriction decreased flow to peritubular capillaries and ^ GFR
excessive constriction: decreased RBF and decreased GFR
explain maximum transport in regards to renal function
for some substances there is a max amount that can be reabsorbed into peritubular capillaries, once the max level is reached the rest is excreted regardless of plamsa concentration
example: hyperglycemia
urine excretion rate formula
urine excretion = filtration - reabsorption + secretion
what does reabsoprtion of water and elctrolytes require?
reabsorption of electrolytes requires ATP (energy)
while water reabsorption is via osmosis and does not require energy
where is the body does the rule, “water follows salt” not always hold up?
in the nephron
main functions of proximal convoluted tubule?
65% of Na, H20, K, Cl, and bicarb reabsoprtion
organic bases, acids, and H ions are secreted into the PCT from peritubular capillaries
main functions of descendign loop of henle?
20% of H20 reabsorbed > concentrates NaCl in the tubular fluid
separates the handling of water and salt
highly permeable to water and only mildly permable to ions
progressive ^ in oxmolarity down the descending loop, starts at 300mOsm/L and gets down to 1,500 mOsm/L in renal pelvis
main function of ascending loop of henle
reabsorbs 20% of tubular sodium
not permeable to H20
this is the countercurrent mechanism
Distal convoluted tubule function
5% of sodium, K, Cl, bicarb reabsorbed
late DCT is imperable to H20 except for in the presence of Aldosterone or ADH
adjusts urea concentration
PTH induced Ca reabsorption occurs here
collecting duct function
5% sodium reabsorption
ADH and aldosterone also work here
ANP inhibits H20 and Na reabsorption
adjusts hydrogen concentration
