Apex- Renal Flashcards
At what vertebral levels do the kidneys lay
between T12-L3 in the retroperitoneal space
The kidney can be divided into what 2 parts and what does each contain (4/2)
Renal Cortex
- Glomerulus, bowmans capsule
- Proximale and distal tubules
Renal Medulla
- loop of henle
- collecting duct
(the two things that drop down)
functional unit of the kidney
nephron
What substance is produced by the juxtaglomeular apparatus
renin
Where is erythropoietin synthesized and what is it secreted in response to?
In the kidney
-secreted in response to hypoxia
The kidney produces : (select 3)
- Calcitrol:
- ADH:
- Aldosterone:
- Renin:
- Erythropoietin:
- Angiotensinogen:
-Calcitrol: parathyroid tells kidneys to convert inactive vitamin D3 to active vitamin D3 (calcitrol)
- ADH: supraoptic nuclei and paraventricular nuclei in the hypothalmus- released from posterior pitutiary gland
- Aldosterone: adrenal cortex
-Renin: by the juxtaglomerular apparatus in response to decreased perfusion
-Erythropoietin: secreted in response to hypoxia
-Angiotensinogen: liver
Where is angiotensinogen manufactured
in the liver
Where is aldosterone synthesizied
in the adrenal cortex
Where is ADH produced/released from
produced in the hypothalmus (supraoptic and paraventricular nuclei)
released from posterior pitutiary gland
Where is erythropoietin syntheized
in the kidney
(in response to hypoxia)
What is calcitrol
the active form of vitamin D3
synthesized in the kidney under influence of parathyroid hormone
where is renin produced from?
the kidney - the juxtaglomerular apparatus
What organs are the regulators of acid base balance
lungs and kidney
lungs- rid body of volatile acids (CO2)
kidneys- rid body of non-volatile acids (Bicarb)
someone is anemic bc of chronic kidney diseae - why are they anemic?
bc the kidney produces erythropoietin (stimulates RBC production), less RBCs = less hgb
Renal blood flow decreases ____% per decade after the age of ____
10% /decade after 50yo
In the neonate, RBF doubles when and reaches adult function when
*rule of 2’s
- RBF doubles in first 2 weeks of life
- adult levels by 2 years
Difference between aldosterone and ADH (vasopressin)
aldosterone controlls extracellular fluid volume (sodium and water reabsorption)
ADH manipulates plasma osmolarity (water is absorbed by sodium is not)
T/F- the kidney is capable of phase 1 and phase 2 metabolism
true
Why do people hgb become elevated when “dry”
bc if they are intravascularly dry, the kidneys sense reduced o2 delivery to them, they secrete erythropoietin to make more RBCs, more RBCs = more hemoglobin to try and carry more o2 to the kidneys
Why cant you give NSAIDs to people with impaired renal function
bc they block prostagladins and prostagladins control blood flow to the renal arteries
- PGE2 and PGI2 vasodilate the renal arteries (afferent)
- Thromboxane A2 consticts the renal arteries (efferent)
- blocking this, impairs filtration time
____ & ____ vasodilate the afferent arterioles
_____constricts the efferent arterioles
(prostagladins subtypes)
PGE2 & PGI2 vasodilate
Thromboxane A2- constricts
What is the vitamin D3 that is sythesized by the skin upon exposure to ultraviolet light?
Calciferol (like a feral cat outside)
-it’s INACTIVE
2 ways we get vitamin D
-how does it become activated?
Sunlight (calciferol, skin) & Diet
(both inactive forms)
- liver converts calciferol to 25-hydroxycholecalciferol (biotransformation- makes orginal word root longer)
25-hydroxychloecalciferol is converted to
1,25- dihydroxycholecalciferol (calcitriol) - active form of vitamin D 3
PTH regulates this process - increase serum PTH, increases serium calcitrol level
Active form of Vitamin D3
Calcitriol
T/F- the renal medulla receives 90% of the renal blood flow
FALSE- renal cortex
-think - cortex = higher level functions = more o2 needed
How do the kidneys prevent hypoglycemia during fasting?
by synthesizing glucose from amino acids
How does active vitamin D3 increase serum calcium levels? (3 ways)
- stimulates intenstines to absorb more CA++ from food
- instructs kidney to reduce CA++ and phos exretion
- Increases deposition of CA++ into the bone (increases bone turnover time- no clue)
What hormone controls plasam osmolarity?
ADH
What hormone controls extracellular fluid volume?
Where do the kidneys receive SNS innervation from?
T8-L1
(Lies at T12-L3)
How much of the CO do the kidneys receive
20-25%
1,000 - 1250ml/min
Of the blood flow delivered to the kidney, only ____% is filtered at the glomerulus
20%
Renal blood flow is (directly/inversely) propotional to the difference between MAP and renal venous pressure and (directly/inversely) propotional to renal vascular resistance
directly proportional to difference between MAP and renal venous pressure (greater pressure gradient = greater RBF)
-inversel ypropotional to RVR (increases resistance = decreased RBF)
Autoregulation maintains renal blood flow between a MAP of ____ - _____
50- 180mmHg
the blood in the peritubular capillaries returns to the IVC by way of what?
the renal veins
How to calculate RBF
(MAP-Renal venous pressure)/ Renal vascular esistance
Renal cortex recieves ___% of RBF (PO2)
Renal medulla recieves ___% of RBF (PO2)
which is more sensitive to ischemia?
Cortex - 90% renal blood flow (PO2 50)
Medulla - 10% RBF (PO2 10)
*medulla is most sensitive to ischemia
T/F - UOP is autoregulated
false- it is linearly related to a MAP > 50
What is the myogenic mechanism and how does it relate to RBF
If pressure is too high through the renal artery, the myogenic mechanism constricts the afferent arteriole to protect the glomerulus from excessive pressure
-
-when the pressure is too low, the mygoenic mechanism dilates the afferent arteriole to increase blood flow going to the nephron
Where in the kidney specifically is the juxtaglomerular apparatus located?
in the distal tubule (specifically the region that passes through the afferent and efferent arterioles)
What renal structures are innervated by the SNS?
The afferent and efferent arterioles
Which factor increases renin release?:
A. PEEP
B. Hypervolemia
C. Angiotensinogen
D. Increased chloride delivery to the macula densa
A. PEEP
Increase or decrease renin release:
-Beta 1 stimulation
Increase (Beta receptors on the juxtaglomerular apparatus)
(Increased/decreased) sodium and chloride delivery to the distal tubule increases renin release
decreased
(decreased solutes, release renin > vasoconstriction)
Aldosterone is a ______ hormone that is produced by the zona ________ of the adrenal gland.
steroid hormone, zona glomerulosa
NA+ reabsorption, K+ and H+ excretion
T/F- Aldosterone does not meaningully affect serum os
true- it manipulates absopriton and excretion of solutes; whereas ADH mainpulates reabsopriton of water (osmolarity) and not solutues
Aldosterone facilitates reabsoprtion and exretion of what?
absorpiton of sodium (and water)
exretion of K & H
think NA has two ++ , so in addition to K+ , it also excretes H+ to balance the scale
Angiotension 2 causes constriction of the (efferent/afferent) arteriole, which (increases/decreases) GFR
efferent
increases
What happens when renin is released
it converts angiotensinogen from the liver to angiotension 1
angiotension 1 is converted to angiotension 2 by ACE in the lungs (also breaks down bradykinins)
- angiotension 2 is the most potent vasoconstrictor in the body: peripheral vessels, efferent arteriole, triggers release of aldosterone (na and water reabosprtion, k & H extretion- DT), relase of ADH (post. pit) - water reabsorption (CD) ; signals sodium to be reabsoprtied in the proximal tubule, and triggers thirst
- wow that was extra
6 mechanisms by which angiotension 2 increases BP
- peripheral vasoconstriction
- constriction of the efferent arteriole
- aldosterone release
- from the adrenal gland (zona glomerulosa)
- steroid hormone
- promotes NA+ reabsoprtion, K+ exretion
- distal tubule
- ADH release
- Posterior pituitary
- water reabsoprtion
- collecting duct
- Na+ reabsoprtion
* proximal tubule - Thirst
What causes aldosterone to be released (3) things
RAAS activation
Hyperkalemia (takes sodium, gets rid of K)
Hyponatremia (takes sodium, gets rid of K)
Conn’s disease occurs with (too much/too little) aldosterone production
too much
- causes sodium retention and potassium loss
- aldosterone = conn man, takes sodium for k
*too little aldosterone production is uncommon
ADH agonizes the (V1/V2) receptor and (increases/decreases) cAMP
agonizes the V2 receptor (increases aquaporin channels in the CDs)
increases cAMP
T/F ADH increases water reabsorption in the proximal tubules
false- collecting ducts
What is the principle determinate of osmolarity
What 2 other things play a role?
Sodium concentration
Glucose and BUN
Normal serum osmolarity
280-290mOsm/L
In what 2 instances is ADH released into the systemic circ?
- increased osmolarity of ECF (will promote water reabsoprtion to dilute solutes)
- decreased blood volume/ RAAS activation
2 ways by which ADH restores blood pressure
1. V1 receptor stimulation in vasculature causes vasoconstriction (increased SVR)
- Gq ⇒ increased IP3, DAG, CA +
2. V2 receptor stimulation in the collecting ducts causes water retention
(Osmolality/Osmolarity) measures the number of osmoles per (liter/kg) of solvent
Osmolality - osmoles per kg
OsmolaRity- osmoles per liteR
(differences are so minuscule that they can be used interchangably but just incase you get questions on this bullshit)
Half life of ADH
5-15 minutes
All of hte following enhance renal perfusion EXCEPT:
- fenoldopam
- PGE2
- Naturitic peptide
- Thromboxane A2
Thromboxane A2
(vasoconstrictor and increases in time of ischemia)
What do naturitic peptides do to the kideny
- well they are released in response to increased blood volume
- so they inhibit RAAS, promoting sodium and water exretion
What does the stimulation of D1 vs D2 receptors result in
D1 ⇒ vasodilation, increased renal blood flow, increased GFR, diuresis, sodium exretion
D2 ⇒ decreased NE release from the presynaptic SNS nerve terminal
3 things that promote renal vasodilation
- prostagladins
- naturitic peptide
- dopamine receptors
Where are prostagladins produced?
inthe afferent arteriole of the kidney
When is arachidonic acid liberated from the cell membrane (4) & How
in response to
- ischemia
- hypotension
- NE
- Angiotension 2
(well thats confusing)
Phospholiapse A2 convers phospholipid in the cell membrane to arachidonic acid
What two things are produced by arachidonic acid and by what 2 pathways
1. Cyclic endoperoxides: (Cyclooxygenase pathway)
- Vasodilators: PGI2 ♦ PGE2 ♦ PGD2
- Vasoconstrictors: Thromboxane A2 ♦ PGF2
2. Leukotrienes (Lipooxygenase pathway)
How do NSAIDS reduce renal blood flow?
By inhibiting cyclooxygenase and the production of vasodilating prostagladins
Vasodilator or vasoconstrictor:
PGI2
Vasodilator
Vasodilator or vasoconstrictor:
PGE2
Vasodilate
(D2, I2,E2)
-when you DIE, you vasodilate
Vasodilate or constrict
PGD2
Vasodilate
(D2, I2, E2)
-when you DIE, you vasodilate
Vasodilate or vasoconstrict:
Thromboxane A2
Vasoconstrict
(+PGF2)
Vasodilate or constrict: PGF2
Constrict
(D-I-E = vasodilate)
(F = fuck that, i’m gonna try to help you not die and constrict)
(+thromboxane A2)
Where are D1 receptors located (2 places)
on the kidney and in splanchic circulation
Where are D2 recpetors present
on the presynaptic adrenergic nerve terminal
(D1/D2) receptor stimulation results in (increased/decreased) cAMP
D1 = increased cAMP (vasodilation, increased RBF, increased GFR, diuresis (bc of the increased RBF), sodium exretion
D2 = decerased cAMP (decreased NE release from presynaptic nerve terminals)
i’m confused
What is Fenoldopam
a selective D1 agonist that increases renal blood flow
- low doses 0.1-0.2mcg/kg/min
- may offer renal protection during aortic surgery and during CPB
2 effects natruetic peptide has on the kidneys
- inhibits renin release
- promotes sodium and water exretion in the collecting ducts
Normal GFR
125mL/min
3 determinants of glomerular hydrostatic pressure
- Arterial pressure
- afferent arteriole resistance
- efferent arteriole resistance
T/F - The Glomerular hydrostatic pressure if the most important determinant of GFR
True
Constriction of the efferent arteriole (increases/decreases) RBF and GFR
decreased RBF but increases GFR
Where does MOST of hte sodium reabsopriton occur in the nephron?
- proximal tubule
- distal tubule
- collecting duct
- ascending loop of henle
Proximal tubule
Define:
Reabsoprtion:
Secretion:
Excretion:
Reabsoprtion - substance is transfered from the tubule > peritubular capillaries
Secretion - substance transferred from the peritubular capillaries > tubules
Excretion - substance is removed fromo the body in the urine
Which part of the loop of henle (ascending vs descending) is highly permeable vs impermeable to water
Descending = highly permeable (think taking a deep dive into a pool of water)
Ascending - impermeable to water
Primary site of reabsorption in the nephron
proximal convuluted tubule
T/F - reabsorption of solutes and water is proportional in the proximal convuluted tubule
True
65% sodium, (followed by) 65% water
+ 65% K, Cl-, HCO3-
Primary goal of the loop of henle
handles sodium and water to form concnetrated or dilute urine
What part of the nephron “fine-tunes” solute concentration
the distal convoluted tubule
T/F- the late distal tubule is impermeable to water
True - except i nthe presence of aldosterone or ADH which fine-tune the final urine concentration