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A&P 2 Test 4 Renal > GFR and GFR Regulation Mechanisms > Flashcards

GFR and GFR Regulation Mechanisms Flashcards

1
Q

True or false GFR is slightly larger in males

A

True

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2
Q

True or false homeostasis requires a near constant GFR

A

True

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3
Q

What would happen if GFR was too fast

A

filtrate in the tubules may pass too quickly and substances may not be reabsorbed

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4
Q

What would happen if GFR was to slow

A

filtrate in the tubules may pass too slowly and all substances may be reabsorbed and waste may not be excreted efficiently

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5
Q

How does renal blood flow (RBF) affect GFR

A

RBF indirectly determines GFR by:

  1. modifying rate of solute and water reabsorption by the proximal tubule
  2. participates in changing concentration of urine
  3. delivers O2 nutrients and hormones to the nephrons
  4. delivers waste for excretion
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6
Q

How does constriction of afferent arteriole affect RBF and GFR

A

decrease RBF and GFR

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7
Q

How does dilation of afferent arteriole affect RBF and GFR

A

increases RBF and GFR

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8
Q

How does constriction of efferent arteriole affect RBF and GFR

A

decreases RBF but increases GFR

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9
Q

How does dilation of efferent arteriole affect RBF and GFR

A

increase RBF but decreases GFR

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10
Q

What GFR is considered stage 1 CKD

A

GFR normal but protein in the urine

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11
Q

What GFR is considered stage 5 CKD

A

GFR <15

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12
Q

What is needed to calculate GFR

A

Serum creatinine, age, race, wt, gender

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13
Q

Why is creatinine used to calculate GFR

A

It is a waste product from normal muscle breakdown that is neither metabolized nor reabsorbed in the kidneys (so freely peed out). In healthy adults the serum level of creatinine should equal the urine creatinine clearance

-if serum level is high, than urine levels/clearance are low because the kidney is not filtering properly

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14
Q

What are the 3 mechanisms that regulate GFR

A
  1. Renal autoregulation
  2. Neural regulation
  3. Hormonal regulation
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15
Q

Renal auto regulatory mechanisms of GFR are constant between what BP

A

90-180 mmHg

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16
Q

What is the target of most renal auto regulation mechanisms

A

variable changes in resistance of afferent arterioles

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17
Q

What are the 2 renal autoregulation mechanisms and what do they respond too

A
  1. Myogenic mechanism =respond to change in BP

2. Tubuloglomerular = respond to changes in Na-CL H2O

18
Q

Describe the myogenic mechanism of renal autoregulation

A
  • BP increase causes stretch in afferent arteriole
  • Causes brief increase in RBF and GFR
  • Smooth muscles of afferent arteriole contract briefly reducing RBF and GFR , this helps to preserve nephron integrity
  • afferent arterioles then adjust resistance to normalize GFR
19
Q

Below 90 mmHg or above 180 mmHg does autoregulation occur

A

No, it is absent

20
Q

Describe juxtaglomerular apparatus

A

a complex structure composed of juxtaglomerular cells (granular cells), macula densa cells, Lacis cells (extraglomerular mesangial cells) that has the ability to affect systemic BP through the tubuloglumerular feedback

21
Q

Where are juxtaglomerular (granular) cells located and what do they do

A

Located in the afferent arterioles

They are modified smooth muscle cells that:

  1. detect low BP (via lack of stretch)
  2. synthesis/store/secrete Renin
22
Q

Where are macula densa cells located and what do they do

A

Located in ascending loop of henle were it meets the afferent arteriole

They:

  1. Detect increase NaCL in the filtrate
  2. When they sense increased solute concentration (meaning high GFR) they release ATP and adenosine which causes contraction of afferent arteriole and extraglomerular mesangial cells
23
Q

Where are extraglomerular mesangial cells located and what do they do

A

Located between the afferent arteriole, efferent arteriole, and late thick ascending loop of henle

Receive signals from other juxtaglomerular apparatus cells and contract or relax as told to

24
Q

Describe tubuloglomerular feedback

A
  • When GFR increases, rate of filtrate through the tubules increase and reabsorption of Na, Cl, and H20 decrease
  • Macula densa cells sense this increased concentration of Na and CL in the filtrate and release ATP and adenosine
  • Extraglomerular mesangial cells, glomerular mesangial cells and the afferent arteriole wall cells react to the ATP and adenosine and constrict which lowers RBF and GFR to normal levels
25
What happens to renal autoregulation when there are large blood pressure or extra cellular fluid volume changes
Hormonal and neural systems play a larger role in GFR regulation, autoregulation can play a role but it is not the key player any more.
26
True or false blood vessels of the kidneys are supplied by the sympathetic and parasympathetic nervous system
False, blood vessels in the kidney (and else where in the body) are only supplied by the sympathetic nervous system.
27
What happens when there is greater sympathetic stimulation throughout the whole body
- Sympathetic stimulation causes EP and NE to be released from adrenal medulla - NE/EP caused afferent arteriole vasoconstriction and reduced RBF because this blood is needed else where - GFR is reduced until autoregulation kick in and normalizes GFR
28
Describe the action of secretion and the hormonal effect of Natriuretic peptide (ANP/BNP)
Secreted by atria or brain in response to increased volume Effects: 1. Dilate afferent arterioles and constricts efferent arteriole 2. Inhibits reabsorption of Na and H2O in the distal convoluted tubules and collecting ducts (so more filtrate is excreted) 3. Inhibits RAAS
29
Describe the action of secretion and the hormonal effect of prostaglandins
Secreted only in response to local hemorrhage or reduced extracellular fluid volume Attempts to counteract vasocontraction of the sympathetic nervous system and Angiotensin II in order to prevent renal ischemia
30
Do prostaglandins effect GFR
No prostaglandins cause a small change in RBF but not enough for GFR
31
Describe the action of secretion and the hormonal effect of nitric oxide
Causes vasodilation at afferent and efferent arterioles Secreted from the endothelium to counteract vasoconstriction of angiotensin II and certain catecholamines
32
Describe the hormonal effect of bradykinin
Vasodilator that stimulates release of nitric oxide and prostaglandins
33
Describe the action of secretion and the hormonal effect of endothelin
Potent vasoconstrictor at both afferent and efferent arterioles Released by endothelial cells of renal vessels, mesangial cells, and distal tubular cells in response to angiotensin II and EP
34
Describe the action of secretion and the hormonal effect of adenosine
Released by macula densa cells of the juxtaglomerular apparatus in tubuloglomerular feedback autoregulation Causes vasoconstriction of afferent arteriole
35
What are the 3 ways the RAAS activated
All 3 causes Renin to be released 1. When there is low perfusion/afferent arteriole pressure 2. Beta 1 adrenergic receptors at the juxtaglomercular cells are stimulated 3. Decrease in Na in the tubule system causes macula dense cells to release ATP/adenosine and start tubuloglomerular feedback
36
Once renin is released describe the actions leading to Angiotensin II activation
1. Renin finds angiotensinogen (protein produced in the liver and regularly released in the blood stream ) and cleaves off a 10 AA peptide converting it to Angiotensin 1 2. Angiotensin 1 is converted to Angiotensin 2 by angiotensin converting enzyme (ACE) in the lungs and the kidneys
37
What are the functions of Angiotensin II
1. Vasoconstrictor that effects both the afferent and efferent arterioles (minor vasoconstriction at efferent first at lower levels then stronger vasocontraction of afferent at higher levels ) 2. Enhances reabsorption of Na, CL, H2O at proximal convoluted tubules 3. Stimulates the adrenal cortex to release Aldosterone 4. Stimulates release of ADH
38
What is the effect of aldosterone on the nephron
Causes principle cells in the collecting ducts to reabsorb Na (water follows) and secrete more K
39
What is the effect of ADH on the nephron
Causes principle cells in the distal convoluted tubules and collection ducts to generate more aquaporin 2 channels in the apical membrane, which causes these cells to become permeable to H2O allowing more H2O to be reabsorbed
40
What are ACE inhibitors used for and how do they work
Used for primary HTN Work by blocking conversion of Angiotensin 1 to Angiotensin 2 . They also increase bradykinin levels which causes vasodilation which increases GFR and offloading extra fluid
41
What is a side affect of ACE inhibitors
Increased bradykinin levels caused by the Rx can cause a characteristic dry cough in some pts
42
What are Angiotensin 2 receptor blockers used for and how do they work
Used to treat HTN, used as a 2nd line treatment to ACE inhibitors Blocks binding of Angiotensin 2 at receptors

A&P 2 Test 4 Renal (7 decks)

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