Flashcards in Osmosis Video Stuff Deck (22)
Cations vs anions
Anions = negative charged molecules
- intracellular = proteins and organic phosphates
- extracellular (both interstitial and plasma) = chloride and bicarbonate
Cations = positive charged molecules
- intracellular = potassium and magnesium
- extracellular (both interstitial and plasma) = sodium
Large negatives charged proteins in the plasma repeal small anions into the interstitial fluid which conversely causes small cations to come into the plasma
- large proteins cant cross but this effect causes the plasma to remain relatively neutral charged
How much of the cardiac output is renal blood flow?
What cells in the nephron secrete renin?
Juxtaglomerular cells in response to low blood pressure
3 layers of glomerular filtration barrier
Separate blood vessels from bowman space
1) endothelium w/ fenestrations
- filters by size
- blocks RBC, solutes and proteins
2) basement membrane
- filters by size and charge
- blocks plasma proteins (albumin)
3) epithelium w/ podocytes and filtration slits
- filters by size and charge
- blocks plasma proteins
What are the three forces that determine the glomerulus pressure?
1) Hydro static pressure of capillary blood (P(gc))
2) hydrostatic pressure of the bowmans space w/ filtrate (P(bs))
3) oncotic pressure of the glomerulus (pi(gc))
Net filtration pressure = P(gc)) - (p(bs)) + (pi(gc))
Why does blood entering the efferent arteriole experience no filtration?
The oncotic pressure in the efferent arteriole reaches zero, which lowers the net filtration pressure
How does changes in the oncotic pressure affect GFR?
High levels = lowers GFR
- increased amount of plasma/blood proteins
Low levels = increases GFR
- decreases amount of plasma/blood proteins
How does changes in the hydrostatic pressure change GFR?
Increases in hydrostatic pressure within bowman space = lowers GFR
- urinary stone blockage
Decreases in hydrostatic pressure within bowman space = increases GFR
How does systemic blood pressure affect RBF?
Increases pressures in renal artery
Decreases resistance in renal arterioles
Both of these two increase GFR and RBF
Two hormones that decrease renal blood flow
- vasoconstriction afferent and efferent arterioles
- decreases GFR and RBF
- released via RAAS system and renin
- vasoconstriction of efferent > afferent
- * this keeps GFR constant, while also lowering RBF
Hormones that increases the RBF and GFR
1) Atrial naturetic peptide (ANP)
- released from atria of heart in response to increased stretching/ high blood pressure
- causes dilation of afferent and constriction of efferent arterioles
- mild increase in RBF, large increase in GFR
- released in sympathetic stimulation often in response to trauma
- dilates both the afferent and efferent arterioles dilate
- increases RBF and GFR
- vasodilator afferent and efferent arterioles
- increases RBF/ GFR
What is the BP range for auto regulation of renal blood flow?
- within this range, myogenic stretch and tubuloglomerular reflex can auto regulate
Why is PAH used to measure true renal plasma flow?
It gets filtered 100%
So plasma PAH = urine PAH+ Venous PAH
Why does excreted PAH increase exponentially initially, but then tapers off into a linear pattern?
Excretion = filtered + secretion
*there is a select number of transport proteins able to take up PAH, whereas filtered is a constant number.*
- so initially both secretion and filtered increase Linearly, which causes excretion to be exponential or steeper increases. However once carrier proteins are fully saturated (Tmax), the secretion tapers off whereas the filtered number is still linear.
- therefore the excretion rate becomes equal to the filtered linear rate.
How does glucose get reabsorbed?
SGLT and GLUT 1/2 receptors in PCT and Thick descending limb
SGLT = apical -> brush border
- uses secondary active transport via energy generated from cotransporter with sodium
GLUT1/2 = brush border to blood
- uses facilitated diffusion
What is the normal blood plasma osmolality?
What happens when osmolarity increases past 300 (usually only occurs in low blood volume)?
1) supraoptic neurons sense this decrease in osmolarity via aquaporin-4 channels and fires signals to the posterior pituitary to release ADH
2) baroreceptors sense decreased blood volume and constrict smooth muscles in vessels to increase blood pressure
3) ADH goes to collecting ducts binds to V2 receptors and upregulated aquaporins to be put into the lumen surface. This causes mass reabsorption of water. In addition, it causes blood vessel lumens to constrict as well
4) hypothalamus stops releasing ADH in decreasing plasma osmolarity (back to normal or even lower)
What is the purpose of the corticopapillary gradient?
To ensure no unnecessary water loss
Is is essentially a osmolarity graident that increases as you get closer to the medulla and is directly tied to the loop of Henle
Where does ADH bind to collecting duct
- converters ATP -> cAMP
Results in 2 actions:
1) increases aquaporins-2 protein production
2) allows for protein vesicles to fuse to cell membrane
What is the function of angiotensin 2
1) causes posterior pituitary to increase production of ADH
2) ADH causes arteries in the body to constrict increasing blood pressure and up regulating aquaporin-2 proteins