Topic 7: Glomerular Filtration and Renal Bllod Flow 2 Flashcards
1
Q
GFR = equation
A
Kf x Net filtration pressure
2
Q
Kf
A
is the glomerular capillary filtration coefficient
3
Q
GFR is determined by what?
A
- the sum of the hydrostatic and colloid osmotic forces across the glomerular membrane which gives the Net Filtration Pressure
- the glomerular capillary filtration coefficient Kf
4
Q
Net Filtration Pressure
A
represents the sum of the hydrostatic and colloid osmotic forces that either favor or oppose filtration across the glomerular capillaries
5
Q
Net Filtration Pressure promotes what?
A
Promotes filtration
- Glomerular hydrostatic pressure (60 mmHg)
- Bowman’s capsule oncotic pressure (0 mmHg) (factor with disease)
6
Q
Net Filtration Pressure inhibits what?
A
Inhibits filtration
- Glomerular oncotic pressure (32 mmHg)
- Bowman’s capsule hydrostatic pressure (18 mmHg)
7
Q
Kf= equation
A
GFR / Net filtration pressure
estimated way to find Kf bc we cant measure directly
8
Q
Kf affected by what ?
A
Affected by overall hydraulic conductivity and surface area of the glomerular capillaries
Not able to measure directly
9
Q
measure of the product of the hydraulic conductivity and SA of the glomerular capillaries
A
Kf
10
Q
Net Filtration Pressure equation
A
Pg-Pb-Pieg+Pieb
11
Q
Normal Kf other capillaries compared to glomerular capillaries
A
Glomerular capillaries Kf is 400x as high as other capillaries.
glomerular capillaries = 4.2 mls/min/mmHg/100 grams of tissue
normal capillaries = 0.01 mls/min/mmHg/100 gm
12
Q
Filtration Coefficient and GFR have what kind of relationship
A
direct positive relationship
13
Q
Increase in Hydrostatic Pressure in Bowmans Capsule (Pb) - does what to GFR
A
Decrease GFR
14
Q
Decrease in Hydrostatic Pressure in Bowmans Capsule (Pb) - does what to GFR
A
Increase GFR
15
Q
Pb a direct means for affecting GFR
A
- Pb is not a primary means for regulating GFR
- Usually not part of day-to-day control of GFR
16
Q
Increase Kf does what to GFR?
A
Increase GFR
17
Q
Chronic uncontrolled HTN and diabetes mellitus do what to Kf
A
decrease Kf
18
Q
Chronic uncontrolled HTN and diabetes mellitus decrease Kf how?
A
increasing the thickness of glomerular capillary basement membrane and eventually damaging the capillary so severely that there is loss of capillary function
19
Q
Increased glomerular oncotic pressure = does what to GFR
A
Decreased GFR
20
Q
How does Increased glomerular oncotic pressure decrease GFR?
A
as blood passes from afferent arteriole through the glomerular capillaries to the efferent arterioles the plasma protein concentration increases 25%. bc 1/5th of the fluid in the capillaries filters into Bowmans capsule concentrating proteins
21
Q
Decreased glomerular oncotic pressure = what GFR?
A
Increased GFR
22
Q
As blood passes through glomerulus plasma oncotic pressure will what?
A
pressure will increase ≈ 20%
23
Q
Plasma oncotic pressure entering and exiting the glomerulus
A
28 mmHg entering glomerulus and 36 mmHg as blood leaves glomerulus
Average 32
24
Q
Factors Affecting Glomerular Oncotic Pressure
A
1) the arterial plasma colloid osmotic pressure
2) Filtration Fraction
25
Filtration Fraction
the fraction of plasma filtered by the glomerular capillaries
26
Increased plasma protein concentration will _____glomerular oncotic pressure which will _____ GFR
Increase glomerular oncotic pressure
| decrease GRF
27
Increased filtration fraction means more whatis being filtered from each ml of blood in the glomerulus
plasma
28
Filtration fraction = equation
GFR / RBF
29
A decrease in RBF (no initial change in GFR) will do what to FF and GFR?
will increase the filtration fraction thus producing a decrease in GFR
30
Increased RBF – __ Filtration Fraction – __ glomerular oncotic pressure – __ GFR
Increased RBF – Decreased Fraction – Decreased glomerular oncotic pressure – Increased GFR
31
Changing RBF with constant glomerular hydrostatic pressure thus has an effect on GFR?
Increase RBF = Increased GFR
| Decrease RBF = Decrease GFR
32
Increased Pg = does what to GFR
Increased GFR
33
Decreased Pg = does what to GFR?
Decreased GFR
34
Pg primary means of changing GFR by? (3)
1. Arterial Pressure
2. Afferent arterial resistance
3. Efferent arterial resistance
35
Increased MAP = what happens to GFR?
Increased
| [Buffered by autoregulation of flow to keep consistent glomerular pressure]
36
Increased Art Pressure does what to Pg and GFR
Increases Pg and Increased GFR
37
Increased constriction (increased Afferent arteriole Resistance) = what happens to pressure (Pg) and GFR ?
Decreased pressure (Pg) = Decreased GFR
38
Decreased constriction (decreased Afferent arteriole Resistance) = what to pressure Pg and GFR
Increased pressure (Pg) = Increased GFR
39
Increased constriction (Efferent Arteriole Resistance) = what happens to Pg and GFR
Increased pressure (Pg)= Increased GFR (slightly)
| as long as RBF doesnt reduce too much
40
Increased constriction (Efferent Arteriole Resistance) = what happens to FF and Glomerular Osmotic Oncotic Pressure
Increased FF and Glomerular Osmotic Oncotic Pressure because of Decreased RBF
41
If Efferent Arteriole Resistance constricts renal blood flow too much what happens?
if constricts too much, GFR decreases bc Renal BF decreases or stops which Increases Glomerularr Colliod Pressure > Pg
42
If Efferent Arteriole Resistance constricts renal blood flow too much what happens to filtration fraction?
Filtration fraction increases (decreased blood flow, increased GFR) which results in higher glomerular colloid oncotic pressure which decreases GFR
43
Increased Bowman hydrostatic pressure (Pb) = does what to GFR?
Decreased GFR
44
Decreased Bowman hydrostatic pressure (Pb) = does what to GFR?
Increase GFR
45
Does Pb normally play a role in controlling GFR?
Normally does not play a primary role in controlling GFR
46
How does an obstruction of the urinary tract cause hydronephrosis?
Bowmans capsule pressure can increase causing serious reduction in GFR a precipitation of the Ca or Uric Acid may lead to stones that lodge in Urinary Tract, that ⬆️ Pb which ⬇️GFR and cause hydronephrosis
47
Obstruction of urinary tract block Pb and GFR?
Could produce big increase in Pb pressure with big decrease in GFR
48
⬇️Kf ➡️⬇️GFR causes
renal disease, diabetes mellitus, HTN
49
⬆️Pb➡️⬇️GFR
urinary tract obstruction
50
⬆️Pie g➡️⬇️ GFR
⬇️ renal BF, increases plasma proteins
51
⬇️Pg➡️⬇️GFR
⬇️ arterial pressure (has only small effect due to autoregulation)
52
⬇️ Efferent arteriolar resistance ➡️⬇️Pg
⬇️ Angiotensin II (drugs that block angiotensin II formation)
53
⬆️Afferent arteriolar resistance ➡️ decreases Pg
⬆️ Sympathetic activity, vasoconstrictor hormones (nori, endothelin)
Decease GFR
54
RBF provides flow for what? (2)
- basic metabolic needs of kidneys
| - excess flow for plasma filtration
55
Renal O2 consumption and blood flow compared to the brain.
O2 consumption is 2x that of the brain
| but blood flow is 7x of the brain
56
Most of O2 consumed by the kidneys is due to what?
supports sodium reabsorption–consumption directly related to rate of sodium reabsorption
57
Renal Oxy consumption is proportional to what?
renal tubular Na reabsorption
58
renal tubular Na reabsorption is related to what?
GFR and rate Na filtered
59
RBF = equation
(Renal artery pressure–Renal vein pressure) / Total renal resistance
60
Percentage of total renal vascular resistance:
| Renal artery ?
100 - 100 = 0%
61
Percentage of total renal vascular resistance:
| Afferent Arteriole ?
~85-60 = 26%
62
Percentage of total renal vascular resistance:
| Efferent Arteriole ?
59-18 = 43%
63
Percentage of total renal vascular resistance:
| Interlobar, arcuate, and interlobular arteries?
8-4= 16%
64
Pg and Glomerular Osmotic oncotic pressure
Resistance of these three areas controlled by sympathetic nervous system, hormones, local control within kidneys
65
% Renal flow going to the renal cortex?
98-99%
66
% Renal flow going to the renal medulla?
only 1-2% of BF, supplied by Vasa Recta (concentrates Urine)
67
Strong Sympathetic Nervous System activation – what effect on renal arterioles ?
can cause constriction to renal arterioles thus
| Decrease RBF and GFR
68
Mild to moderate Sympathetic Nervous System activation - what effect on renal arterioles?
Little effect on RBF or GFR
| moderate decrease in BP with corresponding baroreceptor response
69
When does SNS innervation have the largest effect?
during acute issues, like Brain ischemis and Severe Hemorrage
70
Epinephrine and Norepinephrine effect on RBF?
constrict afferent and efferent arterioles
| Cause decrease in RBF and GFR
71
Endothelium released by what?
-Released by damaged vascular endothelial cells of kidneys and other tissue–
(play role in hemostasis - by vasoconstrict to keep damaged bld in)
72
Endothelium is what? and has what effect on RBF?
- autacoid
- Concentration increased during toxemia of pregnancy, acute renal failure, chronic uremia
- Powerful vasoconstrictor
73
Endothelium does what to GFR?
decreases - bc constriction - ⬇️RBF thus ⬇️GFR .
74
Angiotensin II is what?
circulating hormone and autacoid
| powerful vasocanstrictor
75
Angiotensin II and afferent arterioles (preglomerular vessels)?
```
afferent arterioles (preglomerular vessels) are relatively protected from angiotensin II constriction in most situations associated w/the renin-angiotensin system.
this protection is due to the release of vasodilators (NO and prostaglandins) which counteract that vasoconstriction.
```
76
Angiotensin II and efferent arterioles?
Very sensitive to Angiotensin II
⬆️Angiotensin II -> ⬆️Pg while ⬇️RBF
Enhanced tubular reabsorption because of decreased flow thru peritubular capillaries
77
When is angiotensin II usually formed?
in times where there is ⬇️MAP or ⬇️ Vol which would ⬇️GFR but Angiotensin II prevents the ⬇️GFR by Vasoconstricting.
78
Nitric Oxide basal level important for what?
basal level of NO secreted that helps maintain dilation of renal vessels, to allow kidneys to secrete normal amounts of Na and H2O
79
Nitric Oxide is a what? effect on Resistance and GFR?
autacoid - endothelial derived
| ⬇️ Renal Vascular resistance and ⬆️GFR and urinary excretion of Na
80
Endothelial derived NO
autacoid - that⬇️ Renal Vascular resistance and is released by vascular endothelium throughout the body
81
A NO inhibitor drug does what to GFR and Resistance?
⬆️ Renal Vascular resistance and ⬇️ GFR and urinary Na excretion, The ⬆️Na levels - due to lack of excretion will eventually causing high BP/MAP.
82
Bradykinin & Prostaglandins - impact on RBF and GFR?
- autacoids and hormones
- Potent vasodilators
- Tend to increase RBF and GFR
- Do not appear to have major impact during normal conditions
83
Prostaglandins effect on afferent arterioles
opposing vasoconstriction effect of sympathetic nerves or angiotensin II on the afferent arterioles
May help prevent excessive decreases in RBF and GFR
84
When to Administer nonsteroidal anti-inflammatory agents (ex aspirin)?
-under stressful conditions/bld loss/surgery - -giving this may inhibit prostagladin synthesis may cause significant reduction in GFR
85
Bradykinin & Prostaglandins inhibited by what?
nonsteroidal anti-inflammatory agents
86
Autoregulation of GFR and RBF
- Purpose is to maintain NORMAL GFR and allow control of renal excretion of water and solutes
- Prevents big changes in water / solute excretion with normal changes in blood pressure
87
Autoregulation can last between what MAP pressure ranges?
Decreasing MAP to 75 mmHg or increasing to 160 mmHg results in a small change in GFR (<10% change)
88
If no autoregulation in place and
| Increase MAP 100 to 125 mmHg GFR would do what?
GFR would go from 180 L/day to 225 L/day
89
But urine output and solute excretion DOES what with an increase in MAP
INCREASE
| Pressure diuresis and pressure natriuresis
90
Large increase in urine output prevented by
Autoregulation
| Changes in tubular reabsorption
91
Tubuloglomerular Feedback Mechanism
Links autoregulation of GFR and RBF to the amount of NaCl entering the distal tubule
92
Tubuloglomerular Feedback Mechanism
Regulates RBF and GFR in parallel
| ---GFR regulation rather than RBF regulation plays larger role in maintaining constant delivery of NaCl to distal tubule
93
Tubuloglomerular Feedback Mechanism Components: (3)
Afferent arteriole feedback mechanism
Efferent arteriole feedback mechanism
Juxtaglomerular complex
94
Macula densa cells - where? and what?
Epithelial cells located initial part of distal tubule
| Sense changes in NaCl concentration in the tubular fluid
95
Juxtaglomerular cells surround what?
| in contact with what?
- Surround afferent arteriole where it enters the glomerulus
- Surround efferent arteriole where it leaves glomerulus
- In contact with portion of distal tubule that contains macula densa
96
Juxtaglomerular cells storage site for what?
-Major storage site for renin
97
Juxtaglomerular cells operation
Believed that macula densa monitors amount of volume delivered to distal tubule via NaCl concentration
98
Response from macula densa has two effects
--Dilation of afferent arteriole
Results in an increase in glomerular hydrostatic pressure
--Stimulation of increased renin release from juxtaglomerular cells
Results in an increased constriction of efferent arteriole which produces an increase in glomerular hydrostatic pressure
99
Response from macula densa (decreased concentration of Na Cl in macula densa) has two effects in arterioles:
1. Resistance to BF to afferent arterioles. (Dilation) which increases Pg
2. Increase renin release from the juxtaglomerular cells of the efferent and afferent arterioles.
100
Macula Densa cells sense what?
Sense changes in NaCl concentration in the distal tubular fluid
monitors amount of volume delivered to distal tubule via NaCl concentration
101
GFR decreases - affects Loop of Henle how?
(Flow?
Reabsorption?
Thus concentration in macula densa?)
Flow rate through Loop Henle also decreases
Reabsorption of Na+ and Cl-in loop increases
Concentration Na+ and Cl-at macula densa decreases
Decreased concentration elicits response from macula densa
102
Dilation of afferent arteriole - what happens to Pg?
Results in an increase in glomerular hydrostatic pressure
103
Stimulation of increased renin release from juxtaglomerular cells results in what effect on Pg? (this is a macula densa response)
Results in an increased constriction of efferent arteriole which produces an increase in glomerular hydrostatic pressure
104
An increase in MAP have what reaction to the smooth muscle of small arterioles?
An increase in MAP will cause an increase in smooth muscle contraction especially of small arterioles
BC - MAP increases which cause the vessel walls to stretch thus increasing wall tension. The increased stretch results in movement of additional calcium into the smooth muscle cells which increases the overall level of contraction
105
afferent arterioles show strong or weak myogenic response
afferent arterioles show a strong myogenic response to sudden increase in arterial pressure
(Dont know if this is that important to the kidneys)
106
Result of increased afferent constriction is a reduction in what two things?
reduction in RBF (due to increased resistance) and a decrease in GFR (due to decreased glomerular hydrostatic pressure)
107
Juxtaglomerular Feedback Mechanism
- Feedback mechanism designed to maintain consistent delivery of NaCl to the distal tubule
- Any problem that increases NaCl reabsorption in the proximal tubule will trigger the feedback mechanism
108
Juxtaglomerular Feedback Mechanism:
| two examples?
High protein intake
| Increase in Blood Glucose
109
High protein intake
Higher than normal amino acid concentration in the blood–Sodium and amino acid reabsorption linked, so an increase in amino acid reabsorption --- results in an increase in sodium reabsorption and stimulation of the Juxtaglomerular feedback mechanism
110
High protein intake can increase GFR how much?
20 to 30% increase in GFR 1 to 2 hours after eating a high-protein meal
111
Increase in blood glucose
Again, glucose reabsorption tied to sodium reabsorption
–
As concentration of glucose in the blood increases, glucose and sodium reabsorption also increase thus stimulating the feedback
mechanism which ultimately results in an increase in GFR
