Mechanisms and Control of RBFGFR Flashcards

Question 1

Q

The number of Nephrons decreases with?

Question 2

Q

What is a nephron composed of?

Answer

A

Renal corpuscle

Tubule system

Question 3

Q

What are the components of the renal corpuscle?

What are their functions?

Answer

A

–Glomerulus (glomerular capillaries) - filters blood
–Bowman’s capsule – receives ultrafiltrate

Question 4

Q

Describe cortical nephrons

Answer

A

Short loops of Henle
Surrounded by peritubular capillaries

Question 5

Q

Describe juxtamedullary nephrons

Answer

A

Long loops of Henle
Long efferent arterioles which divided into specialized peritubular capillaries (vasa recta)
Vasa recta aid in concentrating the urine

Question 6

Q

What is the first step in urine formation?

Answer

A

Glomerular filtration

Question 7

Q

•Plasma is filtered under pressure from _____________ into _________________.

Answer

A

glomerular capillaries into Bowman’s capsule

Question 8

Q

•Normally, glomerular filtrate is essentially free of ________________ and ___________, but otherwise identical to plasma

Answer

A

blood cells and proteins

Question 9

Q

How many times do we process our plasma volume each day?

Answer

A

~60 times

Question 10

Q

The glomerular membrane is a molecular sieve that allows… and impedes?

Answer

A

•Free passage of water, small solutes (glucose, amino acids, electrolytes)
–Concentrations are the same on both sides of the membrane
•Impeded passage of large molecules (proteins) and formed elements
•Normally, only very small amounts of protein are filtered into Bowman’s capsule

Question 11

Q

What are the three distinct layers of the glomerular membrane? Highlight the important aspects of each.

Answer

A

Fenestrated capillary endothelium - highly permeable to water, dissolved solutes
Glomerular basement membrane - collagen, proteoglycans contain anionic (negative) charges
Podocyte epithelium - slit pores between podocytes restrict large molecules

Question 12

Q

•Some kidney diseases cause loss of negative charge on the basement membrane before noticeable changes in renal structure
–Minimal Change Disease or Nephropathy

This results in?

Answer

A

–Results in filtration of proteins (esp. albumin) and their appearance in urine (albuminuria or proteinuria)

Question 13

Q

What do you see in more extensive renal injury?

Answer

A

Large amount of protein in urine

Question 14

Q

What 3 physical factors is GFR a product of?

Answer

A

Hydraulic conductivity (Lp) of glomerular membrane (permeability or porosity of capillary wall)
Surface area available for filtration (c. 2 m2)
Capillary ultrafiltration pressure (PUF)

Question 15

Q

What is the product of these two things?

Hydraulic conductivity (Lp) of glomerular membrane (permeability or porosity of capillary wall)
Surface area available for filtration (c. 2 m2)

Answer

A

Product of 1 and 2 is ultrafiltration coefficient K_f

GFR = K_f · P_UF

P_UF= capillary ultrafiltration pressure

Question 16

Q

What is P_UF determined by?

Answer

A

•hydrostatic and colloid osmotic pressures in the glomerular capillaries and in Bowman’s capsule:

• P_UF = (P_GC + π_BC) - (P_BC + π_GC)
or, since π_{BC ~ 0}

P_UF = P_GC - (P_BC + π_GC)

Question 17

Q

Glomerular filtration depends on?

Answer

A

NET filtration pressure

Question 18

Q

•What happens to oncotic pressure as you move from the afferent to efferent arteriole?

Answer

A

Colloid osmotic pressure rises and hydrostatic pressure drops.

This leads to reabsorption

Question 19

Q

What do you think would happen to reabsorption from the tubules if hydrostatic pressure increased within the renal interstitium? What about urinary output?

Answer

A

Reabsorption would be impaired

Urinary output would increase

Question 20

Q

One way to alter GFR is by changing K_f what is changed here? Why?

Answer

A

•things that change surface area or conductivity)
–Altered surface area due to mesangial cell contraction or disease states

Question 21

Q

One way to alter GFR is to modify P_UF, what does this change?

Answer

A

–Renal arterial blood pressure
–Afferent arteriolar resistance
–Efferent arteriolar resistance
•With slight increases in resistance, GFR will increase.
With significant increases in resistance, GFR will decrease.

Question 22

Q

If you change efferent arteriolar resistance the following happen…

•With slight increases in resistance, GFR will increase.
•With significant increases in resistance, GFR will decrease.
Why do these occur?

Answer

A

fluid backs up into the glomerulus
increase resistance so much blood stops flowing into the kidney

Question 23

Q

•Glomerular mesangial cells (M) located within…

Answer

A

glomerular capillary loops.

Question 24

Q

What does contraction of mesangial cells do?

Answer

A

•shortens capillary loops, lowers K_f and, thus lowers GFR.

Question 25

Q

In normal individuals what is GFR primarily regulated by?

Answer

A

alterations in P_GC

Question 26

Q

What is P_CG determined by?

Answer

A

changes systemic arterial pressure (P_A), afferent arteriolar resistance (R_A), efferent arteriolar resistance (R_E)

Question 27

Q

Key concept…

Control of GFR by adjusting…

Answer

A

resistance of afferent and efferent arterioles

Question 28

Q

What happens with afferent arteriolar constriction?

Answer

A

–Greater pressure drop upstream of glomerular capillaries
–P_GC falls, which lowers GFR
–Renal blood flow falls due to resistance

Question 29

Q

What happens with efferent arteriolar constriction?

Answer

A

–Pooling of blood in glomerular capillaries
–Increased PGC increases GFR
renal blood flow - drops

peritubular reabsorption - increases due to decreased hydrostatic pressure

Question 30

Q

What is renal blood flow important for?

Answer

A

•Important in regulation of body fluid volume and solute concentration

Question 31

Q

•Oxygen consumption of renal tissue is higher than that of the brain. Why?

Answer

A

–Related to high rate of active Na+ reabsorption (drives Na+/K+ ATPase)

Question 32

Q

What is the formula for renal blood flow (RBF)?

Answer

A

RBF= (Renal artery pressure-Renal vein pressure)/(Total renal vascular resistance)

Question 33

Q

Vascular resistance to RBF is primarily determined by?

Answer

A

•afferent and efferent arterioles

Question 34

Q

•GFR is strictly regulated over a MAP range between 80 and 170 mmHg via a process called?

Answer

A

autoregulation

Question 35

Q

What are three mechanisms causing vasoconstriction in the renal system?

Answer

A

SNS

Endothelin

Ang II

Question 36

Q

What impact does the SNS have on…

GFR

RBF

Answer

A

•Sympathetic nervous system activation decreases GFR via constriction of the renal arterioles (afferent>>efferent), decreasing RBF and GFR

Question 37

Q

What is endothelin?

Answer

A

•is a peptide hormone (autacoid) released by damaged vascular endothelial cells

Question 38

Q

•Angiotensin II preferentially constricts…

Answer

A

efferent arterioles

Question 39

Q

Where does the sympathetic nervous system primarily influence blood flow in the kidneys? Why?

Answer

A

Primarily causes vasoconstriction at the afferent arterioles since there are far more Alpha 1 receptors there.

Question 40

Q

What effect does Ang II have on renal vasculature at low levels? At high levels?

Answer

A

At low levels it causes vasoconstriction of the efferent capillaries, leading to an increased GFR.

At high levels it leads to a decrease in GFR by constricting both efferents AND afferents.

Question 41

Q

How does ANP affect renal blood flow? What is the impact on GFR?

Answer

A

Dilates afferents

Constricts Efferents

Dilation is more substantial, so a net decrease in renal vascular resistance.

Both effects increase in GFR.

Question 42

Q

What is the role of prostaglandins in RBF?

Answer

A

They cause vasodilation, and modulate the vasoconstriction produced by the SNS and Ang II.

Question 43

Q

In what scenario are NSAID problematic for renal function?

Answer

A

Since they inhibit the synthesis of prostaglandins, the ability of the kidneys to modulate the impact of the SNS and Ang II are diminished. This can lead to a profound reduction in RBF and result in renal failure.

Question 44

Q

What is the myogenic hypothesis of autoregulation of RBF?

Answer

A

states that increased arterial pressure strecthes the blood vessel walls which causes reflex contraction of smooth muscle in the vessel walls and thus increased resistance to blood flow.

Question 45

Q

What is the mechanism of the stretch induced contraction seen in myogenic autoregulation?

Answer

A

The opening of stretch activated Ca2+ channels in smooth muscle membranes. Leading to more tension in the vessel walls.

Question 46

Q

How does the myogenic response equilibrate RBF?

Answer

A

Increased renal arterial pressure stretches walls of afferent arterioles, which contract. This contraction leads to increased arteriolar resistance. The increase in resistance then balances the increase in arterial pressure and RBF is kept constant.

Question 47

Q

What is the other mechanism of autoregulation of RBF?

(Other than myogenic)

Answer

A

Tubuloglomerular feedback.

Question 48

Q

What goes down in tubuloglomerular feedback?

Answer

A

When renal arterial pressure increases both RBF and GFR increase. The increase in GFR results in increased delivery of solute and water to the macula densa region of the early distal tubule which responds by secreting a vasoactive substance (adenosine and ATP as it turns out - not in slides) that constricts afferent arterioles via a paracrine mechanism.

Also worth noting is that the macula densa can detect decreased Na+ levels and produce NO, which serves to vasodilate and counteract the effects of Ang II and the SNS

Question 49

Q

A drop in delivery of NaCL to the macula densa leads to what two things?

What is this related to?

Answer

A

Decreased resistance to blood flow in arterioles.

increased renin release by juxtaglomerular cells - leading to increased ANG II which constricts the efferent arteriole much more than the afferent.

This is related to tubuloglomerular feedback.

Question 50

Q

Where does SNS activation stimulate Na+ reabsorption?

Answer

A

•SNS activation ↑ Na+ reabsorption in proximal tubule, thick ascending limb (LOH), distal convoluted tubule, collecting duct

Question 51

Q

In addition to vasoconstriction of arterioles, what does Ang II do to maintain GFR?

Answer

A

Helps to increase Na+ and H20 reabsorption.

Stimulates aldosterone secretion and the thirst center.

Question 52

Q

What mechanisms cause vasodilation in the kidneys?

Answer

A

Endothelial-Derived Nitric Oxide
Endothelial-Derived Nitric Oxide

Question 53

Q

What is endothelial-derived nitric oxide important for?

Answer

A

–Appears to be important in allowing the kidneys to excrete normal amounts of Na+ and H2O

Question 54

Q

When are
•Prostaglandins and Bradykinin
important in regulating vasoconstriction?

Answer

A

extremely important in regulating the vasoconstriction caused by other mechanisms during situations like volume depletion (or post op)

Question 55

Q

What cells are involved in tubuloglomerular feedback? What does this respond to?

Answer

A

–Responds to increased OR decreased GFR
–Involves macula densa cells, juxtaglomerular cells, extraglomerular mesangial cells

Question 56

Q

Which autoregulatory mechanism is most important in protecting the kidney from HTN induced damage?

Answer

A

Myogenic mechanism

Question 57

Q

What is glomerotubular balance?

What does it do?

Answer

A

•It is an adaptive mechanisms of the renal tubules that cause them to increase their reabsorption rate whenever GFR rises.

It prevents loss of solute

Question 58

Q

•Primary glomerular disease will tend to lower GFR, most often caused by a decrease in net permeability due to loss of filtration surface area.

What autoregulatory response will occur?

Answer

A

Decreased GFR and decreased NaCl leading to TGF activation and a decrease in afferent arteriole pressure to restore GFR

Question 59

Q

•In a patient with hypertension secondary to renal artery stenosis, what would happen to GFR in the stenotic kidney as blood pressure is lowered with an ACE inhibitor?

Answer

A

In a stenotic kidney there is decreased flow, increased myogenic response and decreased GFR. Normally you would see renin release. The ace inhibitor prevents formation of Ang II, and constriction of efferent arterioles, thus preempting GFR maintenance.

Must not give ACE inhibitors to pt. with renal stenosis

Question 60

Q

•How would the following regulatory mechanisms respond to a case of congestive heart failure and a drop in effective circulating volume?

–Ang II
–NE
–Autoregulation
–Prostaglandins

–Why would taking NSAIDS not be advisable?

Answer

A

–Ang II: Constriction of efferents > afferents
–NE: vasoconstrict afferents and efferents to shunt blood to coronary and cerebral vasculature
–Autoregulation: dilate afferent arteriole to increase GFR
–Prostaglandins - vasodilate to prevent renal ischemia

NSAIDS would preempt GFR balance through prostaglandins and lead to renal ischemia

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Mechanisms and Control of RBFGFR Flashcards

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